We tested a conceptual model positing that parent AS would predict child AS, which would in turn predict a latent factor representing children’s pain intensity in response to laboratory pain tasks involving cold, pressure and heat stimuli (see ). The proposed model was not confirmed in the total sample as the path coefficient between parent AS and child AS was not significant (r = 0.12) (). However, further analyses examining the moderating effect of sex on the hypothesized relationships revealed that in girls, parent AS evidenced a significant association with child AS, which in turn predicted the latent factor pain intensity. Mediation analysis revealed that 42% of the effect of parent AS on pain intensity was explained via its effects on child AS in girls. These findings are consistent with our prior work using standard multiple regression analysis that revealed a significant link between parent and child AS in girls but not in boys30
. However, the present study extended these earlier findings by testing the indirect relationship between parent AS and child laboratory pain response through child AS; moreover, the current analyses was able to confirm the existence of a child pain intensity latent factor comprised of pain responses to the three laboratory tasks. One possible reason for the lack of an association between parent and child AS in our sample of boys is that such relationships may be found primarily in clinical samples of boys. In girls, on the other hand, our results suggest that even in healthy samples, the association between parent and child AS holds. Despite the lack of a clear relationship between parent and child AS in boys, child AS was found to be significantly related with pain intensity in the total sample.
Our findings agree with prior research reporting significant associations between parental anxiety and child distress during painful medical procedures 9, 11
, although these earlier studies did not examine sex-dependent effects. Whereas both of these prior studies found that parent anxiety related to upcoming procedures (i.e., anticipatory or state anxiety) predicted child distress, only one 11
reported that parent trait anxiety was related to child distress. Previously, we found that symptoms of anxiety and depression in parents did not evidence significant relationships with child AS, after parent AS was taken into account30
. Thus, we did not include these more general measures of negative affect in the current study. Taken together, our results suggest that parent dispositional factors specifically related to AS, rather than general negative affect, are associated with AS among healthy girls; AS in turn influences how these girls respond to painful stimulation.
The current results support the possibility of sex differences in the transmission of AS from parent to child. It has previously been reported that AS is heritable in women only, with genetic factors accounting for 37% to 48% of the variance in AS among women but, environmental factors accounting for all of the variance in men10
. Several pathways have been posited for the development of AS, including temperamental factors (e.g., behavioral inhibition), insecure attachment36
, and social learning (e.g., instruction by parents)24
. Few empirical studies however, have specifically tested these potential pathways and additional longitudinal research is warranted. Our findings suggest that the environmental factors influencing the development of boys’ AS may not stem directly from parent’s own fear of somatic symptoms but derive from other, unknown sources. In girls, however, the direct association between parent and child AS supports the possibility that, in tandem with genetic effects, environmental influences related to parent AS may help shape the development of their daughters’ AS.
Recent work has revealed that maternal verbal and non-verbal behavior4, 6
directly affect experimental pain responsivity in healthy children. In a study by Chambers and colleagues4
, mother’s behavior during the cold pressor task influenced daughters’ but not sons’ pain intensity during a subsequent cold pressor trial. The authors noted that girls may have been more aware of and reactive to their mother’s behavior during the task than boys—an explanation consistent with research suggesting that girls are more sensitive to parent’s behavior regarding pain symptoms than boys32
. The authors further speculated that parent behaviors may function primarily as signs of parental anxiety or concern which precipitate children’s behavioral distress. Thus, it may be that girls are more sensitive to behaviors reflecting parental anxiety concerning somatic events, compared to boys. This heightened sensitivity in girls, might then lead to their own increased tendency to interpret somatic sensations as dangerous, resulting in elevated reactivity to pain.
It should be noted that our sample consisted of mostly mothers and thus, it is possible that the results may partially reflect a stronger bond among same-sex mother-daughter pairs vs. cross-sex mother-son pairs. The work by Chambers and colleagues4
similarly suggests a more robust mother-daughter relationship in pain-related behavior compared to mothers and sons, fathers were not included in their study. Unfortunately, due to the small number of fathers in the current sample, we were unable to test whether our findings could be attributed to same-sex effects. Moreover, prior research on childhood learning history has not distinguished between the potential influence of mothers and fathers on their sons’ and daughters’AS. Assuming a two-parent family, it is conceivable that such influences may differ and additional studies should include both fathers and mothers to examine possible interaction effects between the sex of the parent and the sex of the child.
The notion that parental AS may influence children’s pain responses is consistent with the conceptualization of AS reflecting beliefs about the dangerousness of somatic symptoms in general, rather than anxiety symptoms per se5
. As mentioned previously, recent investigations have shown that parental informational transmission related to somatic symptoms including pain are associated with high AS 25, 33, 34
indicating that elevated AS may arise from learning to catastrophize about somatic symptoms in general 33
. One area for future study is the extent to which AS leads to increased pain sensitivity to acute, procedural pain. Additional studies might examine how parental transmission of AS may contribute to the development of chronic pain in certain vulnerable children. In light of the known adult female predominance in anxiety and chronic pain disorders, further research may also focus on the possibility that high AS in girls may be a pathway by which such conditions develop and whether there may be certain developmentally sensitive periods (e.g., preadolescence) during which parental AS exerts maximal influence on girls’ AS which may then lead to increased risk for psychopathology in later adolescence or early adulthood.
Several caveats to the current findings should be mentioned. The present data are cross-sectional and therefore, conclusions regarding causality cannot be inferred. Although the current results suggest that our hypothesized model fit the data closely in girls, this does not rule out other possible causal models. Our models focused specifically on child-reported pain intensity and did not include a behavioral measure of pain tolerance. Previous work has indicated that AS does not show a strong relationship with tolerance for experimental pain tasks in adults13
or in children29
. Future studies should examine models incorporating parent-child psychological factors that predict behavioral aspects of pain response (e.g., threshold and/or tolerance). Our analyses revealed a statistically significant indirect relationship between parent AS and girls’ laboratory pain response via girls’ own AS however, the clinical significance of these findings is less clear. Finally, our study does not allow statements regarding mechanisms by which parent AS impact girls’ AS or by which child AS might influence pain response. Future studies may examine how
these pathways operate.
In sum, our findings support the notion that parents’ tendency to interpret anxiety symptoms as dangerous may play a salient role in how healthy girls respond to painful stimuli by influencing girls’ own fear of anxiety symptoms. However, parents’ concerns about anxiety symptoms did not evidence a similar link to their sons’ own fears. Nevertheless, the potential role of AS in shaping children’s response to somatic symptoms was supported by our findings that AS in both boys and girls were predictive of their perceived pain intensity experienced across an array of painful stimuli. The present study was conducted in a healthy sample and the generalizability of our results to clinical samples remains unclear. Nevertheless, one clinical implication of the current findings is that both parents’ and children’s fear of anxiety symptoms may be important targets for evaluation as part of a comprehensive assessment approach in families presenting with pediatric pain problems. Moreover, the possibility that amelioration of AS in parents and their children may lead to reductions in children’s pain response to acute pain stimuli such as that encountered during routine medical procedures should be explored. Potential sex differences in how such interventions might be delivered should also be considered. Thus, it may be that for girls, optimal effects are found when modification of AS is directed at both parents and children, whereas for boys, it may be more appropriate and cost-effective to focus such interventions on children only.