Journal of Developmental and Physical Disabilities

, Volume 23, Issue 3, pp 227–239

Increased Psychopathology in Parents of Children with Autism: Genetic Liability or Burden of Caregiving?

Authors

    • Department of PsychologyCalifornia State University, San Bernardino
  • Charles D. Hoffman
    • Department of PsychologyCalifornia State University, San Bernardino
  • Dwight P. Sweeney
    • Department of PsychologyCalifornia State University, San Bernardino
Article

DOI: 10.1007/s10882-010-9218-9

Cite this article as:
Hodge, D., Hoffman, C.D. & Sweeney, D.P. J Dev Phys Disabil (2011) 23: 227. doi:10.1007/s10882-010-9218-9

Abstract

The goals of this research were to identify which psychopathologies are common in parents of children with autistic spectrum disorders (ASD) and to explore competing hypotheses regarding mechanisms contributing to this risk. By comparing rates of psychopathology in mothers and fathers of children with ASD to rates of psychopathology in parents of typically developing children, this study examined whether increased risk for psychopathology was likely related to genetics or to the burden of caring for a child with a disability. Participants were 269 parents of children with ASD and 446 parents of typically developing children. Mothers and fathers of children with ASD reported significantly more depression, interpersonal sensitivity, paranoid ideation, and obsessive-compulsive behaviors. The pattern of findings suggests that genetic factors, as opposed to caregiving demands, may contribute to the risk for psychopathology in parents of children with ASD.

Keywords

AutismParentingGeneticsCaregiver burdenMental health

Research suggests that raising a child with a disability may adversely affect parental well being (Blacher et al. 1997; Ha et al. 2008; Harris and McHale 1989). Recently, Montes and Halterman (2007) utilized population-based data from the 2003 National Survey of Children’s Health (Blumberg et al. 2005) to compare the psychological functioning and coping of mothers of children with autism to that of mothers of children without disabilities. Based on maternal report for the presence of autism, 364 children, of more than 61,000 respondents in the National Survey, were identified as having autism. Mothers were asked to rate their mental health as either excellent, very good, good, fair, or poor. After controlling for demographic variables and children’s social functioning, mothers of children with autism were more than twice as likely as mothers of other children to report poor or fair mental health. This is consistent with a growing body of research indicating parents of children with autistic spectrum disorders (ASD) are at increased risk for psychopathologies (Abbeduto et al. 2004; Dumas et al. 1991; Lee 2009; Piven and Palmer 1999; Wolf et al. 1989).

Vulnerability for psychopathology in relatives of individuals with ASD was first suggested by Piven et al. (1990) who found high rates of depression among 67 adult siblings of 37 autistic probands. Several studies confirmed elevated risk for depression in parents of children with ASD compared to parents of children with Down syndrome (Abbeduto et al. 2004; Dumas et al. 1991; Piven and Palmer 1999; Wolf et al. 1989) and parents of typically developing children (Dumas et al. 1991; Lee 2009; Wolf et al. 1989). Similarly, parents of children with ASD have been found to be more vulnerable to anxiety than are parents of children with Down syndrome (Piven and Palmer 1999) or parents of children without a disability (Lee 2009). In their meta-analysis of studies conducted between 1973 and 2003, Yirmiya and Shaked (2005) found that parents of children with ASD evidenced significantly more psychopathology overall and specifically in the areas of depression, anxiety, and thought disorder. The first objective of this research was to extend the literature by identifying other psychopathologies to which parents of children with ASD might be vulnerable.

Two possible explanations have been proposed to account for the high rates of psychopathology among parents of children with ASD. One perspective suggests that genes associated with the broader autism phenotype (BAP) are present in family members of children with ASD and predispose these family members to psychiatric illness (e.g., Piven 1999; Piven et al. 1991). The other perspective focuses on the stress associated with the burden of caring for a child with ASD (e.g., Bolton et al. 1998; Olsson and Hwang 2001). This is premised on the well-established relationship between stress and mental health (Bovier et al. 2004; Cohen 2000; Hourani et al. 2006; Kwok and Wong 2000). The second objective of this research was to determine whether psychopathology in parents of children with ASD is more likely related to the BAP or to the burden of caring for a child with ASD. By comparing rates of psychopathology among parents of children with and without ASD and considering how the burden of care may differ for mothers and fathers, the present study was designed to identify the types of psychopathology that may be related to genetics and those that may be related to the burden of caring for a child with an ASD.

Several studies offer tentative support for the position that psychopathology is an expression of the BAP. Research has shown that family members of individuals with ASD have high rates of cognitive disorders such as language delays, spelling disorders, reading disorders, mental retardation (Folstein and Rutter 1977) and peculiar, schizoid-like, personality characteristics (Narayan et al. 1990; Wolff et al. 1988). Moreover, parents of children with ASD often indicate that the onset of their depression (Bolton et al. 1998; Micali et al. 2004; Smalley et al. 1995) or anxiety (Piven et al. 1991) preceded the birth of their child with ASD. Furthermore, Yirmiya and Shaked (2005) found that parents of children with ASD and parents of children with learning disabilities, both of which have genetic liabilities, do not differ significantly in terms of psychopathology. However, both groups of parents evidenced significantly more psychopathology than parents of typically developing children. Presuming a child with ASD is more burdensome than a child with a learning disability, if stress were driving parental mental health, higher rates of psychopathology would be expected in parents of children with ASD. The fact that parents who presumably carried a genetic liability were similar in levels of psychopathology, but more impaired than parents with no known liability (i.e., parents of typically developing children), suggests that genes, rather than stress, are responsible for the elevated psychopathology.

Despite tentative support, Yirmiya and Shaked (2005) and others (e.g., Bölte et al. 2007; Piven and Palmer 1999) have noted that the BAP does not entirely explain the poorer mental health reported by parents of children with ASD. Based on the burden of care hypothesis, it would be expected that child-related factors associated with increased parenting stress would increase parents’ risk for psychopathology. This is particularly relevant as the core characteristics of autism (e.g., cognitive impairments, communication difficulties, self-stimulatory behaviors) have been shown to be associated with stress in parents of children with ASD (Bebko et al. 1987; Hoffman et al. 2008; Tomanik et al. 2004). This is in line with the recent findings of Montes and Halterman (2007) who report that mothers of children with ASD indicated more stress and poorer mental health. Additionally, studies have found that severity of autistic behaviors is associated with parenting stress (Abbeduto et al. 2004; Baker et al. 2002; Bolton et al. 1998; Hoffman et al. 2008; Hoffman et al. 2009; Tobing and Glenwick 2002). Moreover, Yirmiya and Shaked (2005) report that parents of low-functioning individuals with ASD, but not parents of high-functioning individuals with ASD, reported significantly more mental health problems than parents of children with other types of disabilities or parents of typically developing children. Arguably the greater stress associated with rearing a more impaired child could have contributed to the elevated rates of psychopathology among these parents.

Other research supporting the burden of care hypothesis comes from studies comparing mothers of children with ASD to fathers of children with ASD. Mothers of children with ASD report more stress than fathers of children with ASD (Montes and Halterman 2007; Patzold et al. 1998). This may be a consequence of the fact that mothers bear a larger portion of the responsibility of caring for a child with autism (Bristol et al. 1988; Holmes and Carr 1991; Willoughby and Glidden 1995; Wolf et al. 1989). If the strain of rearing an exceptional child is contributing to vulnerability for psychopathology, the burden of care hypothesis predicts that mothers would evidence higher rates of psychopathology than fathers. Studies examining psychopathology in parents of children with ASD are in line with this contention, finding that mothers, but not fathers, of children with ASD have significantly higher scores on depression measures than parents of non-disabled children (Dumas et al. 1991; Olsson and Hwang 2001; Wolf et al. 1989). Additionally, studies comparing mothers of children with ASD to fathers of children with ASD have found that mothers report more depression (Gray and Holden 1992; Lee 2009; Wolf et al. 1989) and more anxiety (Gray and Holden 1992; Lee 2009) than fathers. However, it is unclear whether these differences reflect gender differences found in the general population or a vulnerability for mothers due to the burden of caring for a child with an ASD.

To date there is no conclusive evidence supporting either the burden of care or the BAP hypotheses. It might also be the case that genetics predispose parents to some types of psychopathology and the burden of caring for a child with ASD places parents at risk for other types of psychopathologies. This research sought, first, to determine the specific psychopathologies for which parents of children with ASD are at risk and, second, to identify the psychopathologies that are likely related to the BAP and those likely related to the burden of caring for a child with an ASD. By comparing both mothers and fathers of children with ASD to mothers and fathers of typically developing children, the present study attempted to control for gender differences in rates of psychopathology. Because mothers and fathers of children with ASD share the same level of genetic inheritance with their children, we would expect vulnerability conferred by the BAP to create similarly elevated levels of risk to psychopathology for both mothers and fathers (i.e., no interaction) as compared to mothers and fathers of typically developing children. An interaction, such that mothers of children with ASD are significantly more vulnerable to psychopathology than are fathers of children with ASD, accounting for gender differences, may provide evidence that the increased risk is due to the burden of caring for a disabled child.

Based on previous findings it is predicted that parents of children with ASD will have significantly higher rates of overall psychopathology (e.g., Montes and Halterman 2007; Yirmiya and Shaked 2005) and specifically higher rates of depression (e.g., Abbeduto et al. 2004; Piven and Palmer 1999; Yirmiya and Shaked 2005) and anxiety-related conditions (e.g., Piven and Palmer 1999; Yirmiya and Shaked 2005) than parents of children without ASD. Due to the paucity of research on mental health problems other than depression and anxiety, no predictions were made regarding the other types of psychopathology that were assessed. Furthermore, no predictions were made regarding which psychopathologies are likely to be moderated by parents’ gender.

Method

Participants

All respondents were selected from a larger dataset of families participating in a program of research being conducted at a university in southern California. Only biological parents whose children were living in their homes were eligible for this study. Seven-hundred-fifteen parents participated in this research. Parents of children with ASD included 140 mothers and 129 fathers who had at least one child independently diagnosed with an ASD. Diagnoses were made by licensed mental health professionals (e.g. psychiatrists or psychologists). Additionally, to ensure eligibility for the program each child was reviewed or assessed by the referring agency according to the regulations of the State Department of Developmental Services.

Parents of typically developing children were 302 mothers and 144 fathers. These parents were recruited through the university where students were asked to complete the questionnaire if they met the eligibility criteria (i.e., biological parent of a child living in the home) or have a friend, family member, coworker, or neighbor who did meet the criteria complete the questionnaire. To ensure confidentiality completed questionnaires were returned in sealed envelopes. All students who returned sealed envelopes, even if questionnaires were left blank, were awarded extra-credit that could be applied to a variety of psychology courses offered at the university. This procedure helped to ensure that questionnaires were completed by appropriate respondents and not simply filled in to gain extra-credit. This procedure allowed us to develop a sample of typically developing families that represented the local community as opposed to a sample in which at least one parent was a college student. Because ASD disproportionately affects boys, university students were asked specifically to recruit parents of male children. This precaution was necessary because the rate of autism is approximately four times greater among males than females (Fombonne 2003) and boys with disabilities have been found to be more stressful to parents than girls with disabilities (Korn et al. 1978; Patterson 1980).

Questionnaire packets for parents of children with ASD and parents of typically developing children included an informed consent document. With the exception of demographic questions, for which parents of children with ASD provided extensive information as part of another ongoing project, all parents completed the same series of measures pertaining to parental mental health, as well as other measures related to child and parent sleep habits, family environment, and parental stress. Only demographics and the parental mental health questionnaire were utilized for this study. This research was approved by the university’s institutional review board.

Materials

The Symptom Assessment-45 Questionnaire (SA-45, Maruish 1999)

The SA-45 was selected as a brief, self-report, measure that assesses a wide range of psychopathologies. The SA-45 yields nine subscales, anxiety depression obsessive compulsive, somatization, phobic anxiety, hostility, interpersonal sensitivity, paranoid ideation, and psychoticism. The SA-45 is good indicator of the level of symptomology for each of these symptom domains. The measure also provides a global severity index, derived by summing the subscales, which is a measure of overall level of psychological disturbance.

The SA-45 is a psychometrically sound instrument. According to the manual the SA-45 was normed on a non-clinical sample of more than 1,600 adults and adolescents and a clinical sample of more than 15,000 adults and adolescents (Strategic Advantage, Inc. [SAI], 1998). Coefficients for internal consistency range from.74 to.87 for the non-clinical participants and.73 to.91 for the clinical participants. Test-retest reliability for the non-clinical sample yielded Cronbach’s alphas in the.80s (SAI). Construct validity was demonstrated by Viswesvaran (2001) who reported high intercorrelations between the SA-45 and the SCL-90 (Derogatis et al. 1973) and the Brief Symptom Inventory (Derogatis and Spencer 1982), each a measure of psychopathology.

Results

Sample characteristics for children are presented in Table 1 and sociodemographic variables for parents are presented in Table 2. Groups were comparable except on parental age. Mothers of children with ASD were significantly older than mothers of typically developing children, t(691) = 6.30, p < = .001, and fathers of children with ASD were significantly older than fathers of typically developing children, t(681) = 4.02, p < .001. Parents’ age was controlled for all remaining analyses. Groups did not differ on child’s age, child’s gender, parental marital status, or parental education level.
Table 1

Child characteristics by diagnostic category

 

Children with ASD

Children without ASD

Sample size (n)

269

446

Age

 Range

3–18

3–18

 M(SD)

8.49 (3.20)

8.11 (3.55)

Sex

 Male

78.4%

82.5%

 Female

21.6%

17.5%

Table 2

Parent characteristics by diagnostic category

 

Mothers of children with ASD

Mothers of children without ASD

Fathers of children with ASD

Fathers of children without ASD

Sample size (n)

140

302

129

144

Age

 Range

22–58

21–53

23–79

22–76

 M(SD)

38.34 (7.05)

34.59 (7.72)

40.74 (8.14)

37.94 (8.94)

Marital status

 Married or living with significant other

78.6%

77%

81.8%

81.3%

 Single, divorced, or widowed

21.4%

23%

18.2%

18.7%

Education

 Less than high school completion

7.3%

5.7%

10.2%

11.3%

 High school or equivalent completion

18.7%

16.3%

20%

22.3%

 College, less than BA completion

50%

48.8%

42.6%

42.1%

 College, BA or higher completion

24%

29.2%

27.2%

24.3%

Raw scores from the SA-45 (Maruish 1999) were utilized to assess the level of symptomology for each symptom domain. To examine differences on the SA-45 between parents of children with and without ASD, separate MANCOVAs, in which parental age was controlled, were run for mothers and fathers. Comparisons between mothers were conducted first. Multivariate tests indicated a significant effect of group (i.e., mothers of children with ASD versus mothers of typically developing children) overall on the SA-45 subscales, F(9, 538) = 7.69, p < .01. Post hoc univariate analyses were conducted on each of the SA-45 subscales. Means and standard deviations for these analyses are presented in Table 3. Compared to mothers of typically developing children, mothers of children with ASD reported significantly more anxiety, F(1,548) = 14.57, p < .01, depression, F(1,548) = 34.97, p < .01, obsessive compulsive behaviors, F(1,548) = 19.25, p < .01, somatization, F(1,548) = 8.56, p < .01, interpersonal sensitivity, F(1,548) = 21.19, p < .01, and paranoid ideation, F(1,548) = 5.22, p < .05.
Table 3

Means and standard deviations for parents of children with ASD compared to parents of typically developing children

 

Mothers of children with ASD

Mothers of children without ASD

Fathers of children with ASD

Fathers of children without ASD

Anxiety

8.45 (3.16)**

7.28 (2.87)

7.00 (3.36)

6.85 (2.38)

Depression

10.32(4.43)**

7.91 (3.59)

9.25 (4.60)**

7.47 (3.15)

Obsessive compulsive

9.78 (3.56)**

8.27 (3.45)

9.36 (3.54)**

7.90 (3.15)

Somatization

9.02 (4.22)**

7.72 (3.59)

8.22 (3.77)

7.48 (3.14)

Phobic anxiety

6.60 (4.23)

6.31 (2.63)

6.31 (1.94)

6.01 (2.01)

Hostility

6.72 (2.23)

6.48 (2.88)

6.89 (2.89)

6.72 (2.36)

Interpersonal-sensitivity

9.67 (3.86)**

7.62 (3.29)

8.59 (3.72)**

7.46 (3.34)

Paranoid ideation

8.34 (3.07)*

7.62 (3.20)

8.60 (3.22)*

8.01 (3.06)

Psychoticism

6.10 (1.68)

6.00 (2.04)

6.36 (1.94)

6.22 (1.97)

Mean(Standard Deviation); * p < .05; ** p < .001

For fathers multivariate tests also reveal a significant group difference (i.e., fathers of children with ASD versus fathers of typically developing children) on the SA-45 (Maruish 1999) subscales overall, F(9, 291) = 3.61, p < .01. As with mothers, post hoc univariate analyses were conducted on each of the SA-45 subscales (see Table 3 for means and standard deviations). Compared to fathers of typically developing children, fathers of children with ASD received significantly higher scores on depression, F(1, 301) = 15.42, p < .01, obsessive compulsive behaviors, F(1, 301) = 11.93, p < .01, interpersonal sensitivity, F(1, 301) = 8.44, p < .01, and paranoid ideation, F(1, 301) = 4.14, p < .05.

To test for interactions (i.e., moderation) separate regression analyses, predicting each of the nine subscales scales and the global severity index of the SA-45 (Maruish 1999) were run. Regressions contained parental age, group type (i.e., parent of child with ASD or parent of child without ASD), parents’ gender (i.e., mother or father), and the interaction term for the relationship between group type and parents’ gender. No significant interactions were found, indicating that the strength of the relationship between group type (i.e., parent of child with ASD or parent of non-disabled child) and mental health outcome does not differ for mothers and fathers. That is, scores for psychopathology were higher for parents of children with ASD and higher for mothers in general, however, mothers of children with ASD were not at significantly higher risk than fathers of children with ASD, once gender differences were considered.

Discussion

As predicted, overall, parents of children with ASD evidenced higher levels of psychopathology than parents of typically developing children. Also as expected, both mothers and fathers of children with ASD reported significantly greater depression, respectively, than mothers and fathers of typically developing children. The prediction of greater anxiety-related conditions among parents of children with ASD was only partially confirmed. Both mothers and fathers of children with ASD reported significantly higher scores on the obsessive compulsive and paranoid ideation subscales of the SA-45 than did parents of typically developing children. However, only mothers of children with ASD reported significantly greater scores on the anxiety subscale. Neither mothers nor fathers of children with ASD reported significantly higher scores on phobic anxiety relative to their counterparts.

The preponderance of research on psychopathology in parents of children with ASD has focused on depression. Our findings confirm earlier reports that parents of children with ASD are at elevated risk for depression (e.g., Abbeduto et al. 2004; Dumas et al. 1991; Olsson and Hwang 2001). Much less research has been conducted on anxiety-related conditions. Our results are consistent with studies reporting higher rates of anxiety disorders among family members of individuals with ASD (Piven et al. 1990) and more anxiety in mothers of children with ASD than in fathers of children with ASD (Sharpley et al. 1997). Differences across the types of anxiety assessed (i.e., obsessive compulsive behaviors, anxiety, paranoid ideation, phobic anxiety), highlight the importance of clear operational definitions for anxiety. Additionally, because both mothers and fathers of children with ASD reported elevated obsessive compulsive behaviors and paranoid ideation, but only mothers reported elevated general anxiety, this finding reaffirms the need to consider mothers and fathers separately.

One goal of this research was to contribute to the literature by considering a wider range of psychopathologies than typically assessed in prior studies. To this end, we used the SA-45 which, in addition to depression and anxiety, measures interpersonal sensitivity, somatization, hostility, and psychoticism. Both mothers and fathers of children with ASD reported significantly higher scores than parents of typically developing children on interpersonal sensitivity. Mothers of children with ASD, but not fathers of children with ASD, reported significantly higher scores on somatization than their counterparts with typically developing children. Finally, parents of children with and without autism did not differ on scores for hostility or psychoticism.

The only other study to examine these psychopathologies in parents of children with ASD compared reports on the Symptom Checklist-90-Revised (SCL-90-R; Franke 1995) to normative data on the measure (Bölte et al. 2007). Our findings of increased interpersonal sensitivity in parents of children with ASD, increased somatization in mothers of children with ASD, and no differences across parents on psychoticism are consistent with this earlier research (Bölte et al. 2007). Our finding of no greater risk for hostility in parents of children with ASD is somewhat inconsistent with Bölte et al. who report that 23% of parents of children with autism received scores outside the normal range on the hostility subscale of the SCL-90-R. Nonetheless, the present investigation provides converging evidence that in addition to depression and anxiety, parents of children with ASD may struggle with interpersonal sensitivity and somatization.

To examine the contributions of genetics and the burden of caring for a disabled child, we proposed that psychopathologies which aggregate in parents of children with ASD, but that show similarly elevated rates for both mothers and fathers (i.e., not moderated), would suggest the role of the BAP. The absence of interactive effects for any of the analyses conducted on these psychopathologies suggests that the burden of caring for a child with ASD, which was presumed to fall primarily on mothers, did not contribute to increased risk for these psychopathologies in mothers of these children. The fact that the pressure of rearing a child with ASD was not predictive of psychopathology, suggests that the BAP may be a contributing factor. As parents of children with ASD and parents of typically developing children did not differ in terms of phobic anxiety, hostility, or psychoticism, it appears that these conditions are unrelated to either the BAP or the burden of caring for a disabled child.

Because the burden of caring for a disabled child did not increase the risk of psychopathology for mothers of children with ASD, these findings suggest that genetic factors present in parents of children with ASD may be predisposing them to certain psychopathologies (i.e., depression, paranoid ideation, obsessive-compulsive behaviors, and interpersonal sensitivity). That said, we cannot rule out the possibility that mothers are differentially impacted by the burden of caring for their disabled children but are utilizing coping resources (e.g., social support) relatively less available to fathers. This alternative explanation, that mothers are accessing coping resources, is partially mitigated by previous findings that coping behavior is not related to psycho-social well-being in parents of children with ASD (Gray and Holden 1992). Another possible explanation for the absence of moderation is that, despite the fact that mothers of children with ASD report higher stress (e.g., Montes and Halterman 2007) and greater burden associated with caring for their disabled children (e.g., Bristol et al. 1988; Holmes and Carr 1991; Willoughby and Glidden 1995; Wolf et al. 1989), fathers feel, but are underreporting, similar levels of stress and burden.

The present research benefited from a large sample that included both mothers and fathers with a comparison group that was comparable on many sociodemographic variables that potentially relate to parental psychopathology (i.e., child’s age and gender, parents’ education and marital status). This is significant because child gender has been associated with parental stress (Donovan 1988; Mash and Johnston 1983) and child age has been associated with dysphoria (Dumas et al. 1991) in parents of children with ASD. Importantly, the significant age difference between parents of children with ASD and parents of typically developing children was statistically controlled. This age difference may be attributable to the fact that parents of typically developing children were recruited via college students who are perhaps more familiar with younger aged parents. Another strength of this research is that parents of children with ASD were attending a university-based center and were not specifically recruited for participation in research relating to parental functioning. This procedure may have reduced sample bias.

The present research was limited in that it relied on self-report measures. Previous research indicates that, when completing self-report or structured interview measures, parents of individuals with ASD report poorer mental health than parents of other individuals; however, when clinical diagnostic methods are used, parents of individuals with ASD do not evidence more psychiatric difficulties than parents of other children (Yirmiya and Shaked 2005). Assuming this pattern is true for both mothers and fathers of children with ASD, the use of a self-report measure would not taint the analyses for moderation. Thus, the finding that the burden of caring for a child with ASD did not contribute to the risk for psychopathology should hold despite this methodological limitation. A further limitation of this study is the absence of a burden of care measure. This research inferred that mothers, as primary caregivers, are shouldering a larger burden of caring for their child with ASD. This assumption is based on prior research (Bristol et al. 1988; Holmes and Carr 1991; Willoughby and Glidden 1995; Wolf et al. 1989); however, these studies relied chiefly on subjective measures of caregiving burden. To our knowledge no research has employed an objective measure of parental caregiving burden.

To further explore the burden of care as a risk factor for parental psychopathology future studies should investigate theoretically related variables (e.g., coping, stress, caregiving responsibilities) as potential mediators of the relationship between rearing a child with ASD and parental mental health. To investigate the role of the BAP as a contributor to mental health problems researchers would optimally compare psychopathology in biological parents and non-biological caregivers (i.e., step-parents, adoptive parents) of children with ASD. Psychopathologies that are elevated in biological caregivers relative to non-biological caregivers may be indicative of genetic vulnerability. In contrast, psychopathologies that are equally elevated in biological and non-biological caregivers, compared to caregivers of typically developing children, may offer evidence that the psychopathologies are likely driven by the burden of caring for a disabled child.

To our knowledge this is the only study to test for moderation by gender for psychopathology in parents of children with and without ASD. The lack of moderation evidenced in these findings supports the perspective that the elevated rates of depression, interpersonal sensitivity, paranoid ideation, and obsessive-compulsive behaviors in parents of children with ASD are more likely indicative of the BAP than of the increased burden of caring for a child with ASD. Because the risk for these psychopathologies is elevated similarly for mothers and fathers, the findings highlight the need to further address the mental health of both mothers and fathers of children with ASD. Moreover, this research suggests that some psychopathologies in parents of children with ASD may be unresponsive to interventions aimed at reducing their stress. Additionally, as noted by Piven (1999), an appreciation for the markers of the BAP may allow clinicians and others who work with families of children with ASD to recognize that the behavior of parents of children with autism, which may seem difficult and demanding, is at least in part a manifestation of genetics.

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© Springer Science+Business Media, LLC 2010