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J Pediatr Psychol. 2013 May; 38(4): 365–375.
Published online 2013 January 17. doi:  10.1093/jpepsy/jss131
PMCID: PMC3633252

Individual and Additive Effects of Mothers’ and Fathers’ Chronic Pain on Health Outcomes in Young Adults With a Childhood History of Functional Abdominal Pain

Abstract

Objective To evaluate effects of mothers’ and fathers’ chronic pain on health outcomes in adult sons and daughters with a childhood history of functional abdominal pain (FAP). Method Adults (n = 319; Mean age = 22.09 years) with a childhood history of FAP reported parental history of chronic pain and their own current health (chronic pain, somatic symptoms, disability, use of medication and health care, illness-related job loss). Results Positive histories of maternal and paternal chronic pain were each associated with poorer health in sons and daughters, regardless of child or parent gender. Having 2 parents with chronic pain was associated with significantly poorer health than having 1 or neither parent with chronic pain. Conclusions Chronic pain in both mothers and fathers is associated with poor health and elevated health service use in young adults with a childhood history of FAP. Having both parents with chronic pain increases risk for adverse outcomes.

Keywords: disability, functional gastrointestinal disorder, gender, health service utilization, parents, somatic symptoms

Persistent abdominal pain is common in childhood and, when a medical evaluation yields no evidence of organic disease processes, is termed “functional” abdominal pain (FAP) (Rasquin et al., 2006). The majority of children evaluated for FAP in tertiary care centers meet the symptom criteria for a functional gastrointestinal disorder (FGID), such as irritable bowel syndrome or functional dyspepsia (Baber, Anderson, Puzanovova, & Walker, 2008). Pediatric FAP is often associated with pain-related disability, school absenteeism, and increased health care utilization (Campo, Comer, Jansen-McWilliams, Gardner, & Kelleher, 2002; Hoftun, Romundstad, Zwart, & Rygg, 2011; Saps et al., 2009).

A biopsychosocial perspective on FGIDs (Drossman, 1998) suggests that multiple factors contribute to the etiology and maintenance of FAP. These factors include nondisease alterations in biological factors, such as subclinical immune activation (Collins, 2007), psychological factors, such as pain beliefs and coping (Walker, Baber, Garber, & Smith, 2008), and social contextual factors, such as familial chronic pain. Social learning theory (Levy, 2011; Levy, Whitehead, Korff, & Feld, 2000) and the social communication model of pain (Craig, 2009) suggest that parents may influence their children’s pain experience by modeling pain behavior and reinforcing their children’s pain complaints with solicitous responses (van der Veek et al., 2012; Walker, Smith, Garber, & Van Slyke, 1997).

Research on familial clustering of chronic pain has shown that adults with a positive parental chronic pain history have more frequent pain and less effective endogenous opioid analgesic systems than adults with a negative parental chronic pain history (Bruehl & Chung, 2006; Bruehl, France, France, Harju, & al’Afsi, 2005). Parental chronic pain also has been linked to more frequent pain in children. For example, youth with FAP are significantly more likely to have parents with chronic pain and pain-related FGIDs as compared with youth without FAP (Buonavolontà et al., 2010; Campo et al., 2007; Saito et al., 2008).

Most research on familial history of chronic pain has not specified the gender of family members with a history of chronic pain or has focused exclusively on mothers. For example, Levy et al (2004) found that children of mothers with irritable bowel syndrome (IBS)—a pain-predominant FGID—had more frequent stomachaches, nonabdominal symptoms, school absences, and physician visits than children of mothers without IBS. Others have shown that children of mothers with chronic pain (or poor physical health) have more functional impairment and seek more health care services than peers whose mothers are pain-free (Helgeland, Van Roy, Sandvik, Markestad, & Kristensen, 2011; Kashikar-Zuck et al., 2008; Levy et al., 2004). A related line of research has compared children with and without chronic pain and found that those with chronic pain were significantly more likely to have mothers with poor health as compared with children without chronic pain (Campo et al., 2007; Czyzewski, Eakin, Lane, Jarrett, & Shulman, 2007; Kaufman et al., 1997; Liakopoulou-Kairis et al., 2002; Walker, Garber, & Greene, 1991). The limited research on fathers has found a weak or nonsignificant association between fathers’ pain and their children’s pain (Borge & Nordhagen, 2000; Buonavolontà et al., 2010; Jones, Silman, & Macfarlane, 2004). Thus, whether mothers’ and fathers’ pain is differentially related to pain in their offspring is unknown.

Some evidence suggests that child and parent gender influences the relation between parents’ and children’s pain. Studies examining the relation between family history of pain and individuals’ chronic pain complaints have found sex-dependent effects, with the presence of a familial pain history having a stronger relation to females’ pain than to males’ pain (Edwards, Zeichner, Kuczmierczyk, & Boczkowski, 1985; Fillingim, Edwards, & Powell, 2000). This effect might be explained by sex-dependent genetic factors (Fillingim et al., 2005), social learning (Bandura, 1977), or gender differences in the awareness of pain in others (Koutantji, Pearce, & Oakley, 1998). Additionally, gender schema theory posits that individuals come to perceive, evaluate, and regulate their own and others’ behavior according to the cultural definitions of gender roles (Bem, 1981). Gender role expectations influence pain behavior (Robinson et al., 2001). Thus, maternal pain status may have a stronger effect on daughters than on sons, whereas paternal pain status may have a stronger impact on sons’ than on daughters. No studies to date, however, have tested the hypothesis that the mothers’ and fathers’ chronic pain status is differentially associated with pain complaints in daughters versus sons (Evans et al., 2008).

In addition to the individual impact of each parent’s chronic pain on their children, there is evidence that having multiple first degree relatives (i.e. parents and/or siblings) with chronic pain has an additive effect on the severity of pain and related symptoms in young adults (Edwards et al., 1985; Lester, Lefebvre, & Keefe, 1994). Little is known, however, about the additive impact of parental chronic pain—that is, the effects of having neither, one, or both parents with chronic pain. A recent study (Kaasboll, Lydersen, & Indredavik, 2012) found significant additive effects for parental chronic pain on children’s internalizing emotional symptoms, but it did not investigate effects on children’s pain.

The purpose of this study was to investigate the relation of mothers’ and fathers’ chronic pain histories to the health outcomes in young adulthood of their sons and daughters who had a history of FAP in childhood. We hypothesized that sons and daughters who reported a positive history of parental chronic pain would exhibit more chronic pain, somatic symptoms, disability, and health service use in young adulthood than those who reported no history of parental chronic pain. Moreover, we hypothesized that positive maternal pain histories would have a stronger association with health outcomes in daughters than in sons, whereas positive paternal pain histories would have a stronger association with health outcomes in sons than in daughters. Finally, we hypothesized an additive effect of chronic pain, such that individuals who reported that both parents had histories of chronic pain would report a higher incidence and severity of chronic pain, somatic symptoms, and disability, and health service, as compared with individuals who reported that only one or neither parent had chronic pain.

Method

Participants

This study reports data on parent chronic pain that were collected as part of a comprehensive evaluation of health outcomes of pediatric patients with chronic functional abdominal pain; other aspects of the evaluation have been reported elsewhere (Dengler-Crish, Bruehl, & Walker, 2011; Dengler-Crish, Horst, & Walker, 2011; Walker, Dengler-Crish, Rippel, & Bruehl, 2010; Walker, Sherman, Bruehl, Garber, & Smith, 2012). Participants in the baseline evaluation were consecutive new patients, aged 8–18 years, who presented to a tertiary pediatric gastroenterology clinic for evaluation of abdominal pain between 1993 and 2004 (Walker, Smith, Garber, & Van Slyke, 1997; Walker, Garber, Smith, Van Slyke, & Claar, 2001; Baber, Anderson, Puzanovova, & Walker, 2008). Patients were eligible for participation in the baseline evaluation if they lived with parent(s) or parent figure, reported abdominal pain of at least 3-months’ duration, had no history of chronic illness or disability, and no organic disease diagnosis for abdominal pain from the referring physician. Participants were eligible for the follow-up study of health outcomes if they were aged ≥12 years, at least 4 years had elapsed since initial study enrollment, no evidence of significant organic disease was found in the medical evaluation at the tertiary clinic, and they reported no major chronic disease (e.g., inflammatory bowel disease, multiple sclerosis) at follow-up.

The sample was drawn from a database of 760 former participants who met eligibility criteria for age and follow-up interval. They were sent letters with a card to return to decline further contact. Among these, 6 declined contact, leaving 754 potential participants. Of these, 261 (34%) could not be located, 54 (7%) declined participation (primarily because of lack of time), 40 (5%) could not be scheduled, 3 were excluded because of recent onset of chronic disease, and 5 were excluded because of missing data, leaving a follow-up sample of 391 participants, representing 51% of those eligible for the follow-up assessment. Participants and nonparticipants in the follow-up assessment did not differ significantly on sex, age, or baseline pain severity. The current study included only participants who were aged ≥18 years (n = 319) at the follow-up assessment, as younger participants did not provide data on parental chronic pain. The majority of participants were female (65.8%) and Caucasian (92.1%). They were young adults at follow-up (mean age = 22.09 years; standard deviation [SD] = 3.18 years; median age = 21.00 years). Of the participants who reported on their student status (n = 260), 34.8% were currently students at follow-up. Those who were not students at the time of assessment (n = 148) reported a mid-range socioeconomic status of 31.30 (SD = 14.45) based on the Hollingshead Index.

Procedure

Data for the study were obtained by telephone interview administered by trained interviewers. Participants were read the questions, informed of the answer response choices, and provided their responses over the telephone. Participants responded to the interview in a private place to ensure privacy and confidentiality. Informed consent was obtained from all participants, and the study was approved by the Vanderbilt Institutional Review Board.

Measures

The Persistent Pain Questionnaire assessed history and location of chronic pain (Bruehl et al., 2005). Participants were asked to identify locations of both current and lifetime chronic pain based on the standard eight body locations described by the International Association for the Study of Pain (for the purposes of this study, the abdominal pain site was excluded because the Rome III Questionnaire provided assessment of the established diagnostic criteria for FGIDs associated with abdominal pain). For each site, participants were asked if they had experienced chronic pain daily or almost daily for the past 3 months. If they responded positively to this question, they were asked to rate their current pain intensity on a scale of 0–100. Participants were considered to have current nonabdominal chronic pain if they rated a current nonabdominal pain site at ≥30.

Participants also provided proxy reports regarding parental chronic pain. They were asked whether their biological mother and biological father had ever “experienced chronic pain daily or almost daily for ≥3 months.” Separate variables representing mothers’ and fathers’ chronic pain were coded (0) “no history of chronic pain” and (1) “history of chronic pain.” In addition, a single variable representing the number of parents with chronic pain was coded (0) neither parent with a history of chronic pain, (1) only one parent with a history of chronic pain, or (2) both parents with a history of chronic pain. If participants did not know the chronic pain history for a parent, they were excluded from study analyses specific to that parent.

The Abdominal Pain Index (API) consists of four items assessing the weekly frequency (rated on a 6-point scale from not at all to every day), daily frequency (rated on a 6-point scale from none to constant), duration (rated on a 9-point scale ranging from no pain to all day), and typical intensity (rated on an 11-point scale ranging from no pain to the most pain possible) of abdominal pain episodes over the past 2 weeks (Walker, Smith, Garber, & Van Slyke, 1997). All items were converted to a 5-point scale, and a composite score was created yielding a mean ranging from 0 to 4. Alpha reliability for the API in this study was .67.

The Children’s Somatization Inventory (CSI) was designed to evaluate the severity of 35 somatic symptoms experienced during the past 2 weeks (Walker, Beck, Garber, & Lambert, 2009; Walker et al., 1991). Participants reported how much each symptom bothered them on a 5-point scale ranging from 0 to 4. The items were summed, yielding a total score ranging from 0 to 140. Alpha reliability for the CSI was .87 in this study.

The Functional Disability Inventory (FDI) assessed difficulty in physical and psychosocial functioning because of physical health (Claar & Walker, 2006; Walker & Greene, 1991). Participants reported how much difficultly they would have performing 15 activities because of their physical health on a 5-point scale ranging from 0 to 4. The items were summed, yielding a total score between 0 and 60. Alpha reliability for the FDI was .87 in this study.

The Rome III Diagnostic Questionnaire for Functional Gastrointestinal Disorders assessed the Rome III symptom criteria for abdominal pain related FGIDs, including irritable bowel syndrome, functional dyspepsia, and functional abdominal pain syndrome (Drossman & Dumitrascu, 2006). Participants answered 24 questions regarding their symptoms during the past 3 months and were classified according to whether they met criteria for an abdominal pain related FGID at follow-up.

The Health Service Utilization Questionnaire was developed for this study to assess participants’ recent health service utilization, medical diagnoses, and use of prescription medications. For the purposes of this study, two specific outcomes were assessed as indicators of high levels of health service utilization: (i) use of four or more prescription medications; and (ii) whether the participant had been admitted to an emergency room in the past 3 months.

Job loss secondary to illness was assessed by asking participants to report whether they ever quit or lost a job because illness interfered with their ability to work.

Hollingshead Index of Socioeconomic Status (Hollingshead, 1975) was based on occupation and level of education. Scores can range from 8 (unskilled laborer) to 69 (professional).

Data Analysis

All data analyses were conducted using IBM SPSS version 19.0. Frequency analyses examined participants’ reports of each parent’s pain history (yes, no, do not know). Participants who responded “do not know” regarding their maternal or paternal chronic pain history (maternal chronic pain history: n = 29; paternal chronic pain history: n = 64) were excluded from analyses pertinent to that parent (i.e., participants who responded “do not know” for one parent but provided a response for the other parent were retained in analyses for the appropriate parent). The distributions of scores on the measures of somatic symptoms (CSI) and functional disability (FDI) violated the assumption of normality; therefore, these measures were logarithmically transformed for analyses, but untransformed means are reported in the tables.

To examine the relation between parental chronic pain history and participant gender, we conducted two 2 × 2 chi-squares (Maternal Chronic Pain History × Child Gender; Paternal Chronic Pain History × Child Gender). Analysis of variance (ANOVA) analyses for participant gender (2) by maternal chronic pain history (2) examined the relation of maternal chronic pain history and gender to levels of abdominal pain, somatic symptoms, and disability. These analyses were then repeated with paternal chronic pain history substituted for maternal chronic pain history.

Logistic regression analyses examined the interactive effects of maternal chronic pain history and child gender on dichotomous health outcomes at follow-up, including the presence of a FGID, nonabdominal chronic pain, current prescription for four or more medications, visit to the emergency room within the last 3 months, and illness-related job loss. These analyses were then repeated with paternal chronic pain history substituted for maternal chronic pain history.

To examine the additive effects of mothers’ and fathers’ chronic pain, we conducted a one-way ANOVA evaluating the association of parental chronic pain history (coded as neither, one, or both parents) to the participant’s levels of abdominal pain, somatic symptoms, and disability. Post hoc comparisons were conducted using the Fischer LSD test. Finally, we conducted logistic regressions examining the relation of parental chronic pain history (neither, one, or both parents) to dichotomous health outcomes at follow-up including the presence of a FGID, nonabdominal chronic pain, current prescription for four or more medications, visit to the emergency room within the last 3 months, and illness-related job loss.

Results

Frequency of Maternal and Paternal Chronic Pain Reported by Sons and Daughters

The majority of participants (n = 154; 53.1%) reported that their mothers had a history of chronic pain, and slightly more than one-third (n = 104; 40.8%) reported that their fathers had a history of chronic pain. A significantly greater proportion of female than male participants (45.5% vs. 32.2%) reported that their fathers had a history of chronic pain, X2 (1, 255) = 4.22; p = .04. Female participants also reported slightly higher rates of maternal chronic pain than male participants (57.0 vs. 45.4%), but this difference did not reach statistical significance, X2 (1,290) = 3.51; p = .06.

Relation of Maternal History of Chronic Pain to Health Outcomes in Sons and Daughters

Table I presents the means and standard deviations of health outcomes as a function of parental chronic pain history and participant gender. Participants with a positive history of maternal chronic pain reported significantly higher levels of abdominal pain [F(1, 286) = 19.38, p < .001], somatic symptoms [F(1, 286) = 16.20, p < .001], and disability [F(1, 286) = 20.32, p < .001] as compared with participants with a negative history of maternal chronic pain. Gender had a significant main effect on levels of abdominal pain [F(1, 286) = 31.64, p < .001], somatic symptoms, [F(1, 286) = 24.89, p < .001], and disability [F(1, 286) = 13.56, p < .001], with females reporting higher levels of symptoms and disability than males. However, results revealed no significant gender × maternal chronic pain interactions.

Table I.
Means and Standard Deviations for Health Outcomes by Parental Chronic Pain History and Gender

Table II presents the percent of participants with specific dichotomous health outcomes as a function of parental chronic pain history. Logistic regression analyses showed that participants who reported a positive maternal history of chronic pain, compared with those reporting a negative maternal history of chronic pain, were 3.18 (95% confidence interval [CI]: 1.31, 7.75) times more likely to meet diagnostic criteria for a clinically significant FGID, but they did not differ on the presence of nonabdominal chronic pain, current prescription medication use, having visited the emergency room (ER) in the past 3 months, or illness-related job loss. No significant main effects emerged for participant gender or for the interaction of maternal chronic pain history with participant gender. The relation of maternal chronic pain to health outcomes did not differ significantly for sons and daughters.

Table II.
Percent of Participants With Maternal and Paternal Chronic Pain Histories Meeting Criteria for Various Outcomes

Relation of Paternal History of Chronic Pain to Health Outcomes in Young Adults

Similar to the findings for maternal history of chronic pain, participants with a positive history of paternal chronic pain reported significantly higher levels of abdominal pain [F(1, 251) = 25.39, p < .001], somatic symptoms [F(1, 251) = 28.46, p < .001], and disability [F(1, 251) = 15.02, p < .001] as compared with participants with a negative history of paternal chronic pain, Table I. Gender had a significant main effect on levels of abdominal pain [F(1, 251) = 25.39, p < .001], somatic symptoms, [F(1, 251) = 18.60, p < .001], and disability [F(1, 251) = 11.22, p = .001], with female participants reporting higher levels of abdominal pain, somatic symptoms, and disability than male participants. However, results revealed no significant gender × paternal chronic pain interactions.

Results from logistic regression analyses yielded significant main effects for paternal chronic pain history (see Table II). Specifically, participants who reported a positive paternal chronic pain history, in comparison with participants who reported a negative paternal chronic pain history, were 4.38 (95% CI: 1.67–11.47) times more likely to meet diagnostic criteria for a clinically significant FGID, 7.20 (95% CI: 2.46–21.05) times more likely to report the presence of nonabdominal chronic pain, such as back or limb pain, 9.60 (95% CI: 1.02–90.21) times more likely to currently have four or more prescription medications at the time of follow-up, and 9.39 (95% CI: 1.81–48.68) times more likely to have lost a job because of illness during the time interval since study enrollment. Main effects for paternal chronic pain history on ER visits in the past 3 months yielded nonsignificant results. Significant main effects for participant gender indicated that female participants were 2.36 (95% CI: 1.10–5.07) times more likely to meet diagnostic criteria for a clinically significant FGID than male participants. Main effects for participant gender on nonabdominal chronic pain, prescription medication, ER visits, and job loss were nonsignificant. No significant interaction effects emerged for paternal chronic pain by participant gender. The relation of paternal chronic pain to health outcomes did not differ significantly for sons and daughters.

Additive Effect of Positive Chronic Pain History for Neither, One, or Both Parents

We examined the additive effects of mothers’ and fathers’ chronic pain for the subset of participants (n = 249; 78% of total sample) who provided responses regarding both parents (summarized in Figure 1). Number of parents (0, 1, or 2) with a positive chronic pain history was significantly associated with higher levels of abdominal pain [F(2, 246) = 17.30; p < .001; η2 = .12], somatic symptoms [F(2, 246) = 19.54; p < .001, η2 = .14], and disability [F(2, 246) = 15.93; p < .001; η2 = .11]. Post hoc comparisons revealed that all three groups (i.e., those with a positive chronic pain history for both parents, those with a positive chronic pain history for one parent, and those with a negative chronic pain history for both parents) significantly differed from each other on levels of abdominal pain and somatic symptoms (all p-values <.05). Specifically, participants with a positive chronic pain history for both parents reported significantly higher levels of abdominal pain (M = 1.68, SD = 1.04) and somatic symptoms (M = 21.27, SD = 13.88) as compared with those with a positive chronic pain history for one parent (abdominal pain: M = 1.17, SD = 0.85; somatic symptoms: M = 13.01, SD = 9.07), who in turn reported significantly higher levels of abdominal pain and somatic symptoms as compared with participants with a negative chronic pain history for both parents (abdominal pain: M = 0.84, SD = 0.88; somatic symptoms: M = 10.82, SD = 8.41). For functional disability, participants with a chronic pain history for both parents reported significantly greater levels of disability as compared with those with a positive chronic pain history for one parent or a negative chronic pain history for both parents (M = 8.03, SD = 8.96 vs. M = 3.61, SD = 5.26 vs. M = 3.18, SD = 5.13; p < .05), but the latter two groups did not differ significantly from each other.

Figure 1.
Severity of abdominal pain, somatic symptoms, and disability by parental chronic pain history. Note. *p < .05; ns = not significant; CP HX = chronic pain history.

Additionally, participants who reported a positive chronic pain history for both parents, compared with participants with a negative chronic pain history for both parents (see Table III), were 2.73 times more likely to meet diagnostic criteria for a FGID at follow-up, 4.29 times more likely to report the presence of nonabdominal chronic pain, such as back or leg pain, 2.94 times more likely to currently have four or more prescription medications at the time of follow-up, 3.36 times more likely to have visited the emergency room in the past 3 months, and 3.06 times more likely to have lost a job because of illness during the time interval since study enrollment. Moreover, participants who reported a positive chronic pain history for one parent, compared with participants with a negative chronic pain history for both parents, were twice as likely to meet diagnostic criteria for a FGID at follow-up, but did not differ in their likelihood to report the presence of nonabdominal chronic pain, have four or more prescription medications, have visited the emergency room in the past 3 months, or have lost a job because of illness.

Table III.
Odds Ratios and Confidence Intervals Comparing Participants With a Positive Chronic Pain History for Neither, One, or Both Parents

Discussion

In addition to replicating the previously observed association between chronic pain in mothers and their children (Buonavolontà et al., 2010; Campo et al., 2007; Saito et al., 2008; Venepalli, Van Tilburg, & Whitehead, 2006), this study demonstrated a significant association between chronic pain in fathers and their children. Specifically, in our sample of young adults with a childhood history of FAP, positive histories of chronic pain in mothers and fathers were each independently associated with adverse health outcomes in their sons and daughters in adulthood. Adverse outcomes associated with maternal and paternal chronic pain included clinically significant abdominal pain, as defined by the Rome III criteria for FGIDs, somatic symptoms, and disability. A positive history of chronic pain in fathers also was associated with nonabdominal chronic pain, greater prescription medication use, and illness-related job loss in their sons and daughters in adulthood. Our findings underscore the importance of maternal and paternal histories of chronic pain in the long-term health outcomes of pediatric FAP.

This study also demonstrated, for the first time, additive effects of maternal and paternal history of chronic pain on health outcomes in their children. Specifically, young adults who reported having two parents with a positive history of chronic pain had significantly poorer health outcomes as compared with those who reported having one parent or neither parent with a positive chronic pain history. This finding may indicate a dose–response relationship where increased exposure to parental pain and pain behaviors may correspond to higher levels of children’s pain and related impairment. In our study, young adults who reported one parent with a positive chronic pain history had less severe pain and disability than young adults who reported two parents with a positive chronic pain history. Notably, young adults who reported one parent with a positive chronic pain history still had elevated pain severity and somatic symptoms in comparison with those who reported a negative chronic pain history for both parents, but did not differ from this group regarding functional disability. This could reflect the impact of having at least one pain-free model of activity on young adults’ pain-related disability.

The significant relation between parent and child chronic pain might be explained by genetic or contextual factors. One study found that individuals with a positive parental chronic pain history exhibited impaired endogenous opioid analgesic responses to acute pain, suggesting that this biological impairment in pain modulatory mechanisms might have a heritable component (Bruehl & Chung, 2006). Family context also may influence children’s pain experience. For example, a twin study found that having a mother with IBS or a father with IBS, independently, were stronger predictors of IBS than having a dizygotic (DZ) twin with IBS (Levy et al., 2001). Because DZ twins and their parents should share roughly the same amount of genetic material, this finding suggests that, in comparison with genetic heritability, social learning or modeling of illness behavior may have an equal or greater effect on the development of IBS.

Although several studies, including the present, have found a significant relation between chronic pain in parents and their children, researchers have yet to examine parents’ pain behaviors that may serve as a model for their children (van der Veek et al., 2012). It is possible that a parent may experience chronic pain, but not display observable pain behaviors in the presence of their child. Future research should evaluate both parental pain behaviors and children’s perceptions of parental pain behaviors to better assess the potential role of modeling as a mechanism affecting the relation between parent and child pain. Other biological characteristics, such as genetic factors and central sensitization to pain, should also be investigated in both parents and children to understand their potential contribution to this relation.

Although other studies have found a significant relation between perceptions of parental pain and pain in daughters, but not sons (Evans, Tsao, & Zeltzer, 2008; Fillingim et al., 2000), our study did not replicate these effects. It is difficult to untangle specific reasons for the differences in our findings because study designs and samples differed a great deal. Similar to a previous study (Koutantji et al., 1998), we found daughters were more likely than sons to report a paternal history of chronic pain. However, our study further showed that the relation between chronic pain in parents and their children was similar for sons and daughters (i.e., parental chronic pain was associated with higher levels of abdominal pain, somatic symptoms, and disability in both sons and daughters).

The findings from the current study should be interpreted in light of several limitations. The study used a cross-sectional design and assessed parental chronic pain with retrospective reports by their children who were young adults at the time of assessment. A study by Bruehl et al. (2005), comparing offspring and parent report of parental chronic pain history, found high sensitivity values, indicating offspring generally tended to accurately report parental chronic pain histories. However, recall bias is possible, in that young adults with higher disability and health service use may have been biased towards over-reporting pain in their parents. Real time studies with objective measures of parent illness behavior as well as both offspring and parent reports of parental chronic pain and behaviors are needed to extend the findings of this study. Additionally, the current study did not assess the onset or duration of the parents’ chronic pain. Drawing from literature on risk for psychopathology in children of depressed mothers (Goodman & Gotlib, 1999), it is possible that children who are older at the age of onset of parental chronic pain may be less vulnerable to adverse effects. As might be expected, some of our participants did not know the chronic pain status of one or both of their biological parents, perhaps because of adoption or to lack of contact with a parent after divorce. It is possible that the relation between parent and child chronic pain, as well as possible gender effects, may differ depending on whether a child was raised in a single- or two-parent home and amount of contact with the parent. The current study, however, did not have information on family composition. Finally, the results from the present study were based on young adults with a history of FAP who originally presented to a tertiary care facility and may not generalize to those who present to primary care facilities or do not seek treatment for their abdominal pain.

The current study has at least two implications for clinical practice. First, when evaluating a child with chronic pain, equal attention should be paid to the potential impact of both maternal and paternal chronic pain histories. A child from a family in which both parents have a history of chronic pain may be at particularly high risk for adverse health outcomes. Second, our finding that parental chronic pain, especially chronic pain in fathers, is associated not only with increased severity of their children’s pain and disability but also to their increased use of prescription medications suggests that the clinical evaluation should include assessment of health care beliefs and practices in parents with chronic pain.

Funding

This research was supported by R01 HD23264 from the National Institute on Child Health and Human Development and does not represent official views of the Institute. Support also was provided by: Vanderbilt Kennedy Center (P30 HD15052), Vanderbilt Digestive Disease Research Center (DK058404), and the Vanderbilt CTSA (1 UL1 RR024975) from the National Center for Research Resources, National Institutes of Health.

Conflicts of interest: None declared.

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