Psychological Bulletin 2002, Vol. 128, No.

5, 746 773

Copyright 2002 by the American Psychological Association, Inc. 0033-2909/02/$5.00 DOI: 10.1037//0033-2909.128.5.746

The Association Between Psychopathology in Fathers Versus Mothers and Childrens Internalizing and Externalizing Behavior Problems: A Meta-Analysis
Arin M. Connell and Sherryl H. Goodman
Emory University
In light of the selective focus on maternal (vs. paternal) psychopathology as a risk factor for child development, this meta-analysis examines the relative strength of the association between psychopathology in mothers versus fathers and the presence of internalizing and externalizing disorders in children. Associations were stronger between maternal than paternal psychopathology and the presence of internalizing (but not externalizing) problems in children, with all average effect sizes being small in magnitude. Relations were moderated by variables that highlight theoretically relevant differences between psychopathology in mothers versus fathers (e.g., age of children studied, type of parental psychopathology) and by variables related to methodological differences across studies (e.g., method of assessing psychopathology in parents and children, type of sample recruited, familial composition).

In the 27 years since Lamb (1975) referred to fathers as the forgotten contributors to child development (p. 245), developmental psychologists have made impressive strides in furthering the fields understanding of the impact fathers have on the lives of their children. Although a large body of evidence now documents paternal influences in normal child development (for an overview of this sizeable literature, see Lamb, 1997), researchers interested in the development of child behavior problems have been slow to catch up. In the examination of factors associated with the risk for behavioral problems in children, mothers have received the lions share of research attention. Studies examining the characteristics of mothers in association with child behavior problems have traditionally done so to the relative exclusion of fathers, leaving a large gap in the understanding of fathers potential role in the development and maintenance of child behavior problems (Phares, 1992). Improved understanding of the impact of fathers on child psychopathology is critical given that fathers not only contribute directly and indirectly to child development through their caretaking and their contributions to the family context in which development occurs, but also contribute 50% of their childrens genes (Phares & Compas, 1992). Thus, failure to consider fathers in research on the development of child behavior problems is likely to leave a large proportion of the variance in child outcomes unaccounted for, or worse, incorrectly attributed solely to mothers. The recognition of this oversight in the literature is not new. As early as 1961, Eron, Banta, Walder, and Laulicht recognized the disregard of paternal influences in the development of child aggression as a major methodological flaw in the literature. In 1985, Caplan and McCorquodale reviewed 125 articles published in nine clinical journals in the years 1970, 1976, and 1982 and found pervasive evidence of mother-blaming in the literature.

Correspondence concerning this article should be addressed to Arin M. Connell or Sherryl H. Goodman, Department of Psychology, Emory University, Atlanta, Georgia 30322-2470. E-mail: aconnel@learnlink .emory.edu or psysg@emory.edu 746

Whereas 72 forms of child psychopathology had been attributed to mothers in the literature, none had been attributed to fathers. Furthermore, mothers were mentioned in relation to the development of specific problems in their children five times as often as were fathers, and mother child interaction was investigated in 77% of the articles, whereas only 49% examined father child interaction. More recently, Phares and Compas (1992) reviewed 577 articles published in eight clinical and developmental journals between 1984 and 1991 and concluded that the percentage of articles including fathers had not changed significantly during that time period. Forty-eight percent of the articles had focused exclusively on mothers, whereas only 1% had included only fathers. Just 26% of the articles had included both parents and analyzed them separately. Phares and Compas concluded that the mother-blaming approach to child psychopathology was still prevalent, with paternal influences dramatically overlooked in the attempt to understand the development of behavior problems in children. This lack of attention has been attributed to both methodological and sociocultural factors (Phares, 1992). Methodological factors that make the study of mothers easier than the study of fathers include the assumption that fathers are less willing to participate in research than are mothers; the idea that certain adult disorders such as depression, the most commonly studied form of parental psychopathology, are more prevalent in women than in men; a higher likelihood of women than men with a psychological disorder (e.g., schizophrenia) to marry and have children; and that the high incidence of divorce results in a large number of children living in mother-headed households or in stepfamilies rather than with their biological fathers (Cancian & Meyer, 1998; Phares, 1992; Watt, 1986). Larger barriers to the inclusion of fathers in research have been sociocultural norms and theories of child development that have placed primary emphasis on maternal influences on both normal and abnormal child development. At the cultural level, societal norms have emphasized the caregiving role of the mother in the

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lives of children, while largely relegating fathers to the role of breadwinner. In line with this view, research has consistently shown that mothers are overwhelmingly more involved than fathers in child care both in single- and dual-earner families (Lamb, Pleck, Charnov, & Levine, 1987). Theories of familial influences on child development, from psychodynamic to behavioral orientations, have mirrored the traditional cultural images of mothers and fathers in placing primary emphasis on the quality of the mother child relationship while largely downplaying paternal influences (for a review, see Lamb, 1997). In the years since Phares and Compass (1992) review, however, researchers have begun to recognize and respond to this gap in the literature such that there now exist sizeable bodies of research on both maternal and paternal factors associated with the development of internalizing and externalizing behavior problems in children. The growth of this body of research marks an important step in furthering the understanding of the development of emotional and behavior problems in children, an important endeavor given the number of children and adolescents who develop such problems. Estimates of the percentage of children and adolescents exhibiting clinically significant internalizing or externalizing problems in the general population range from 7% to 22% (Anderson & Werry, 1994; Verhulst & Koot, 1992). Research has demonstrated that both dimensions are associated with a range of negative outcomes including peer rejection, impaired social cognitive development, the development of academic problems, and difficulty with emotion regulation (for a review, see Cicchetti & Toth, 1991). Externalizing problems carry additional societal implications, as children with externalizing problems are at an elevated risk for delinquency and for criminal behavior in adulthood (Kazdin, 1987; Robins, 1978). In the present review, we focus on the broadband syndromes of internalizing and externalizing disorders rather than examining specific narrowband childhood disorders for two primary reasons. First, comorbidity within both internalizing disorders (anxiety and depression) and externalizing disorders (oppositional defiant disorder [ODD], conduct disorder [CD], and attention-deficit/hyperactivity disorder [ADHD]) is extremely common. Indeed, rates of comorbidity between depression and anxiety as high as 50 75% have been found in studies of children and adolescents in both community and clinical samples (Biederman, Faraone, Mick, & Lelon, 1995; Kashani et al., 1987; Masi, Mucci, Favilla, Romano, & Poli, 1999). Similarly, for externalizing disorders, roughly one third to one half of children who meet criteria for CD or ODD also meet criteria for ADHD, although rates of comorbidity as high as 75% have also been found (Biederman, Newcorn, & Sprich, 1999; Stewart, Cummings, Singer, & DeBlois, 1981). Second, the vast majority of studies have not controlled for the co-occurrence of disorders in children by using pure cases (i.e., children only meeting diagnostic criteria for one disorder). In light of the high rates of comorbidity, results from studies focusing on pure cases of disorders in children may be of limited generalizability to the general population of children experiencing problems (although such studies do contribute valuable information regarding the validity and specificity of different childhood disorders). By focusing on broadband syndromes, the present review may provide a more generalizable, albeit less detailed, picture of the present state of the literature regarding the association between psychopa-

thology in mothers and fathers and the presence of emotional and behavioral problems in children. In studying the emergence of emotional and behavior disorders in children, researchers have often relied on a high-risk design, in which children at a known risk for a disorder are examined in detail. One of the most commonly studied risk factors for internalizing and externalizing problems in children is the presence of psychopathology in one or both parents. For reasons discussed previously, however, the bulk of this research has focused explicitly on psychological disturbance in mothers as a risk factor for children. Research on children of mothers with depression, anxiety, or schizophrenia has revealed a broad range of disturbances in children (Bergman & Walker, 1995; Goodman & Gotlib, 1999; Merikangas, Avenoli, Dierker, & Grillon, 1999; Watt, 1986). Although fewer studies have focused on paternal psychopathology, qualitative reviews by Phares and Compas (1992) and Phares (1996) have found that paternal depression is associated with a range of negative outcomes in children, whereas paternal alcoholism, substance abuse, and antisocial behaviors are associated with externalizing behavior problems in children, particularly among clinical rather than community samples.1 However, less consistent evidence was found for similar associations with internalizing problems in children. One of Phares and Compass (1992) central recommendations for future research on the impact of parental psychopathology on child functioning was that greater emphasis be placed on conducting separate analyses of the associations with mothers and fathers to examine whether certain types of parental psychopathology may exert different influences on the development of emotional and behavior problems in children depending on the gender of the parent. The growth of the literature that has examined both maternal and paternal mental health problems as risk factors for the development of internalizing and externalizing behavior problems makes this an appropriate time to examine the question of the differential impact of paternal and maternal psychological problems on child functioning in detail. As yet, there has been no quantitative review of the literature on the relative impact of mental disturbance in mothers and fathers, though Dierker, Merikangas, and Szatmari (1999) have noted that studies comparing the effects of psychopathology in mothers versus fathers for children have generally yielded inconsistent results. In qualitative attempts to review these findings, Dierker and colleagues argued that children are equally affected by the presence of depression in mothers versus fathers, but Luthar, Cushing, and McMahon (1997) summarized evidence indicating that depression in mothers is more strongly associated with disturbances in child functioning than depression in fathers. Similarly, Dierker and colleagues found evidence that alcoholism may exert larger or smaller effects depending on the gender of the affected parent, though the direction of the difference appeared inconsistent. Luthar and colleagues found that alcoholism and substance abuse in fathers may be more closely associated with behavior problems in children than similar problems in mothers, at least in African American samples. One of
1 One exception to the mother-dominated focus of the high-risk studies is research on parental alcohol and substance abuse, which has tended to focus more heavily on fathers, likely because of the greater prevalence of such disorders in men (Phares, 1996; Phares & Compas, 1992).

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the singular advantages of a quantitative review is the ability to provide clarity to an area of the literature that has proven difficult to examine in a qualitative fashion. Though the principal goal of the present review is not to examine the mechanisms through which parental psychopathology might be associated with the presence of internalizing and externalizing problems in children, a consideration of the potential mechanisms of risk helps to form specific hypotheses about whether certain forms of psychopathology may be more or less strongly associated with child disturbance depending on the gender of the affected parent. Goodman and Gotlib (1999) proposed four mechanisms through which maternal depression may be associated with maladaptive developmental outcomes for children, including (a) genetic transmission, (b) the development of dysfunctional neuroregulatory mechanisms (especially resulting from prenatal experiences associated with maternal psychopathology), (c) exposure to the mothers maladaptive affect, behavior, and cognitions, and (d) contextual stressors associated with depression in mothers. Although Goodman and Gotlibs model was developed to explain the effects of maternal depression on the emergence of child psychopathology, the broad parameters of their model may be applied more widely to the effects on children of different types of psychopathology in both mothers and fathers. In discussing these mechanisms, we examine hypotheses at two levels. General hypotheses for which the mechanisms lead to the same general prediction for all forms of psychopathology in parents are discussed first. For mechanisms in which the type of psychopathology is relevant in framing hypotheses, these specific hypotheses are discussed second. In conducting the meta-analysis, the type of psychopathology in mothers and fathers is treated as a moderator to examine whether the type of psychopathology is related to the differential effects for mothers and fathers. Given that both parents contribute 50% of their childrens genes, genetic transmission of parental psychological disturbance may predict that psychopathology in either mothers or fathers should be equally associated with the presence of emotional and behavioral disturbance in children. However, the prediction of equal influence of mothers and fathers from genetic transmission is predicated on the assumption that disorders are equally heritable in males and females. For disorders in which genetic risk is gender specific, genetic transmission may result in larger effect sizes for the parent in whom the disorder is more closely related to genetic factors. For most forms of psychopathology, however, there do not appear to be clear differences in heritability for males and females. One possible exception is for alcoholism (but see Heath, Slutske, & Madden, 1997), which Cloninger, Bohman, and Sigvardsson (1981) have classified into two subtypes associated with variations in gender-specific heritability. Type I alcoholism (milieu-limited) is moderately heritable for both males and females, whereas Type II alcoholism (male-limited) is strongly associated with genetic factors in male offspring and is associated with an early age of onset and with elevated rates of externalizing forms of behaviors in fathers (Cloninger, Sigvardsson, & Bohman, 1996). Given that Type II alcoholism appears to be more strongly mediated by genetics, paternal alcoholism may be more closely associated with the presence of behavioral disturbances in children (especially sons) than alcoholism in mothers. The second proposed mechanism of transmission is that parental psychopathology may be associated with complications during the

offsprings prenatal development, which result in a range of problems that place the infant at risk. Researchers have linked a variety of forms of maternal psychopathology, including depression, anxiety, substance and alcohol abuse, and schizophrenia, or their correlates (such as poor prenatal care), with adverse conditions during prenatal development. Adverse conditions include fetal exposure to neuroendocrine correlates of mothers depression or stress and teratogenic consequences of exposure to drugs or alcohol. Support for concerns about fetal development comes from evidence of increased risk for preterm delivery, low birth weight, growth retardation (including decreased head circumference and brain growth), problems with neuroregulation (especially of the hypothalamic-pituitary-adrenal axis), and behavioral problems during early infancy including irritability, difficulty being soothed, diminished responsiveness, and lower levels of activity (e.g., Bennedson, Mortensen, Olesen, & Henricksen, 1999; Coles, Platzman, Smith, James, & Falek, 1992; Field, 1992; Glover, 1997; Hedegaard, Henriksen, Secher, Hatch, & Sabroe, 1996; Zuckerman, Bauchner, Parker, & Cabral, 1990). Given that this mechanism relies on the effects of psychopathology or its correlates on the intrauterine environment, the relatively clear prediction for all of the disorders is that maternal psychopathology, if evident during the offsprings fetal development, should be more closely associated with the presence of behavior problems in children than paternal psychopathology. However, the ability to test support for this mechanism is limited to the extent that studies report whether the mothers disorder was present during her pregnancy with the child. The third proposed mechanism of transmission is that children are exposed to parents maladaptive affect, behavior, and cognitions. This mechanism is associated with several possible predictions. First, given that mothers are overwhelmingly the parent most responsible for child-rearing activities (for a review, see Pleck, 1997), it is likely that children are exposed more to the maladaptive behaviors, affective disturbances, and cognitive distortions associated with psychopathology in mothers than in fathers. If quantity of exposure is the critical factor, maternal psychopathology in general should be more closely associated with internalizing and externalizing problems in children than paternal psychopathology. Conversely, however, if Lamb (1997) is correct in his argument that the amount of time that fathers invest in child care is less closely associated with child outcome than the quality of fathers involvement with their children, then the gender of the affected parent would not necessarily be related to variations in the magnitude of risk to children. Another possibility associated with this third mechanism of transmission is that parents may exert more influence on children of the same gender. From a social-learning standpoint, justification for this possibility is drawn from Banduras (1977) conclusion that children are more strongly influenced by models of greater similarity to themselves. In addition, the influence may be bidirectional, as parents may be more likely to identify with children of the same gender, resulting in a greater investment of time and energy in them. Consistent with these arguments are several studies that have found that parents exert the greatest influence on same-sex children, whether through their negative parenting style (e.g., Deater-Deckard & Dodge, 1995; Koestner, Zuroff, & Powers, 1991) or through the presence of depressive symptoms in mothers versus fathers (Hops, 1992). Taken together, these results

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lend credence to the notion that parental mental health problems may be more strongly related to behavior problems in same-sex children. As such, child gender is examined as a potential moderator. The above hypotheses deal with the presence of psychopathology in general; however, it is also possible that specific disorders are differentially related to disturbances in parenting by mothers versus fathers. Indeed, there is some evidence that depression in women may be more closely associated with disrupted parenting quality than depression in men. Jacob and Johnson (1997) found that depression in mothers was more closely associated with parent child negativity during a problem-solving task than was depression in men. Similarly, Field, Hossain, and Malphurs (1999) found that depressed fathers displayed higher quality interactions (i.e., were more active, more positive, and more facially expressive and displayed more game playing and higher quality vocalizations) with their 3 6-month-old infants than depressed mothers. Field and colleagues argued that these differences in interaction quality between depressed mothers and depressed fathers could be related to the more active coping style of depressed men than of depressed women or to the more playful style of interaction displayed by men in general with their children, which may compensate for the presence of depression on their style of interaction. Taken together, these results lead to the hypothesis that maternal depression may be more closely associated with childrens behavior problems than paternal depression because of the greater parenting disturbances displayed by depressed women than depressed men. For other disorders, there is little evidence regarding potential differences in parenting by affected men and women, and thus there is little basis for forming specific hypotheses. The final mechanism proposed to explain the association between parents psychopathology and behavior problems in their children is that contextual stressors associated with psychopathology in mothers and fathers may be related to the development of emotional and behavior problems in children. Although there is a great deal of research linking psychopathology in adults with sources of contextual stress, including familial disruption, marital discord, and economic pressure, there is little work comparing the relative strength of such associations in men and women. It is likely that psychological disturbance in both parents is associated with elevated levels of contextual stress, though the nature of that stress may vary for men and women. Several authors have suggested that psychological distress in women may be more closely associated with familial sources of stress than psychological distress in men because relationship considerations may be more centrally related to womens self-perceptions than to mens, whereas males may be more affected by economic and societal pressures than women (Almeida & Kessler, 1998; Culp & Beach, 1998; Dehle & Weiss, 1998). However, the implications of different forms of stress for the emergence of behavior problems in children has been the subject of little study; therefore, the final mechanism provides little basis for predicting differences in the relations between psychopathology in mothers versus fathers and the presence of emotional and behavioral problems in children. Although the bulk of the discussion up to now has focused on examining how the mechanisms of transmission of psychopathology in parents lead to predictions of differential effects of psychopathology in mothers and fathers for childrens functioning, there are also several other factors that may moderate the association

between parental psychopathology and childrens functioning, and we examine these as well. The first such moderator is the age of the children in the studies. As articulated by Rothbaum and Weisz (1994), there are two contrasting hypotheses regarding the potential influence of age: that effect sizes are larger for younger children and that effect sizes are larger for older children. Researchers from a variety of domains have argued that parents exert their greatest influence when children are very young, the general thinking being that there are fewer competing influences in the lives of young children. In addition, because early childhood is a time of tremendous learning and growth, younger children may be more susceptible to parental influence than older children. Conversely, several theories of child development have argued that the mutual influences of parents and children on each other tend to develop over the course of years (Maccoby, 1992; Patterson, 1982). Thus, the congruence between parent and child behavior may be greater in samples using older children. The results of Rothbaum and Weiszs meta-analysis examining the association between parenting behaviors and externalizing problems in community samples supported this latter conclusion, with larger effect sizes found in samples that examined older children. A third possibility, however, is that age effects differ for fathers and mothers. The small body of research examining the level of father involvement in child care has yielded somewhat inconsistent evidence regarding differences in fathers involvement in caring for younger versus older children, though some of the inconsistency may be due to the manner in which father involvement is conceptualized and measured (for a review, see Pleck, 1997). In a longitudinal study, Bailey (1994) found a large increase in the level of fathers participation in caregiving activities with their children from infancy to 5 years of age. In line with this finding, it is possible that fathers take a more active role in caregiving as children mature, such that one might expect to see larger associations between paternal psychopathology and child behavior problems in samples studying older children. Conversely, as mothers levels of involvement in child care are relatively more stable than fathers, it is possible that the strength of association between maternal psychopathology and childrens behavior problems are unrelated to the age of children studied. The second moderator we examine is the year of study publication. The date of publication is of interest primarily because of the claim already discussed, namely that the levels of father involvement in child care have risen in recent years, reflecting the changing cultural expectations for fatherhood (Pleck, 1997). It is possible that with rising levels of father involvement in the lives of their children, paternal mental disturbance would be more strongly related to child disturbance in studies conducted more recently. Finding larger effect sizes for more recent studies may tend to support this contention, though such a finding would also be consistent with other possible explanations, such as changes in research or assessment methodology. Third, the composition of families studied is examined as a moderator because results for mothers and fathers from intact and nonintact families may differ. Mothers typically retain custody following divorce (Seltzer, 1991); therefore, it is possible that maternal mental health problems are more strongly related to childrens problems in single-parent families because single mothers may experience higher rates of stress and children may have less exposure to a healthy alternative caregiver. Conversely, al-

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though many fathers remain actively involved with their children following separation or divorce, fathers may have less contact with their children and as such may exert less influence on childrens functioning (Suleman & Meyers, 1999). Until now, we have mentioned potential moderators that are associated with predictions of differential relations between psychopathology in mothers versus fathers and childrens functioning. The final moderators, however, are not associated with specific predictions of mother versus father differences. Rather, we expect these variables to moderate the magnitude of the associations between psychopathology in both mothers and fathers and internalizing and externalizing problems in children in the same manner. Thus, although these variables are expected to moderate the magnitude of effect sizes in general, they are not associated with specific predictions of mother versus father differences. The first of these moderators is the nature of the sample included in the study. Two types of samples are generally used in psychopathology research, either clinical or community samples. Clinical samples are generally recruited from treatment clinics and typically consist of families who are seeking mental health services. Though clinical samples are extremely useful in that they provide an efficient means to collect data on children with problems who may be relatively hard to find otherwise, there is a question as to the generalizability of the results from clinical samples, as there may be systematic differences between individuals who do and do not enter the mental health service system (Goodman, Lahey, Fielding, & Dulcan, 1997). In line with this notion, Goodman and colleagues (1997) compared mentally disordered children and adolescents from a population-based sample who either had or had not received outpatient mental health services in the prior year and found that children who had received treatment were more severely impaired, more likely to have comorbid disorders, more likely to be Caucasian, had more educated parents, and were more likely to be postpubertal if female. Similar concerns exist for samples of referred parents, as studies comparing clinical versus community samples of adults have found that adults from clinical samples are likely to have higher rates of comorbidity (Galbaud du Fort, Newman, & Bland, 1993), to be more severely impaired, and to have higher rates of disorders in first degree relatives (Kendler, 1995) than adults from community samples. Because of the greater severity of disturbance in clinical samples of children and parents, as well as the higher rate of disorder in first degree relatives from samples of parents, we expected that clinical samples would yield larger effect sizes, in general, for both maternal and paternal psychopathology than community samples. We also explore possible differences in childreferred versus parent-referred samples to examine whether there are systematic differences in effects from these two types of clinical samples, although there is little firm basis for making specific predictions. Similarly, the use of a diagnostic versus a symptom-based approach to the identification of parental psychopathology and child behavior problems are examined as potential moderator variables, although there is little basis for predicting larger or smaller effect sizes from either approach to assessment. For some disorders, such as those for which diagnoses are relatively rare in one gender (e.g., antisocial personality disorder [ASPD] in women), there may still be substantial variation in symptom levels that are associated with child adjustment, and thus it is possible that

symptom-based studies may show stronger effects than diagnostically based studies. As this possibility is speculative, however, these moderator analyses should be considered exploratory. Furthermore, for both diagnostically and symptom-based studies, the source of the ratings of childrens problems may be an important moderator. For symptom-based studies, which commonly rely on parent, child, or teacher reports of childrens behavior, research has consistently found that reports of behavior problems are often discrepant across different raters (Achenbach, McConaughy, & Howell, 1987; Briggs-Gowan, Carter, & SchwabStone, 1996; Sawyer, Streiner, & Baghurst, 1998). Such discrepancies may result from several factors including that parents may be more sensitive to the presence of emotional and behavior problems in their children than are raters from outside the family, such as teachers, or that childrens behavior may vary from home to school environments such that discrepant reports reflect actual behavioral discrepancies across situations (Sawyer et al., 1998). A third possibility is that the presence of psychopathology in parents may bias their reports of internalizing and externalizing problems in their children, leading to an overreporting of such problems. However, studies addressing the presence of biased reporting by psychologically distressed parents have yielded mixed findings (Breslau, Davis, & Prabucki, 1988; Briggs-Gowan et al., 1996; Jensen, Traylor, Xenakis, & Davis, 1988; Richters & Pellegrini, 1989; Sawyer et al., 1998). Most recently, in a large-scale study of families with children aged 10 11 or 14 15 years, Sawyer and colleagues (1998) concluded that psychological distress had a small but generally significant effect on mothers and fathers reports of emotional and behavioral problems in their children. In line with this finding, we predicted that larger effect sizes for both maternal and paternal psychopathology would result from studies in which parents are the sole raters of behavior problems in their children. Research has also focused on differences across informants for studies examining childrens diagnoses, which commonly gather information from parents, children, or medical records. Results of such research suggest that although crossinformant agreement tends to be low (as for symptom-based studies), ratings from different sources tend to be clinically relevant even when discrepant (e.g., Bird, Gould, & Staghezza, 1992; Jensen et al., 1999). Thus, we explore whether differences across diagnostic informants may be related to differences in the magnitude of effects found, although there is little solid basis for forming specific predictions. Similarly, we examine the informant for parental diagnoses as a possible moderator. Several approaches to diagnostic assessment of parents have been used in the literature, including direct diagnostic interviewing, indirect assessments through interviews of spouses or other family members, and reviews of medical records. It is possible that the approach to assessment may be particularly related to the magnitude of effects for fathers, as fathers may be less likely to be directly involved in research than mothers, for reasons discussed. In such cases, mothers may serve as the indirect informant on paternal diagnoses. Results from such studies may either underestimate or overestimate the effects of paternal psychopathology, as mothers may be biased to either underreport or overreport problems in their husbands. Because little research has examined such possibilities, however, we conduct these analyses in an exploratory manner.

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The final moderator we examine concerns the use of samples in which the biological statues of parents is known versus unknown. Although a number of researchers have focused exclusively on the association between psychopathology in parents and their biological children, the majority of studies in the literature have either included both biological and nonbiological parents in their samples or ignored this dimension altogether, presenting no information on the biological status of mothers and fathers. Given that internalizing and externalizing disorders are significantly heritable (see, e.g., Eaves et al., 1997), it is likely that studies focusing exclusively on the biological offspring of mothers and fathers yields stronger effects for the presence of psychopathology in parents and children.

tively, these studies involved over 60,000 parent child dyads. Sample sizes ranged from 17 to 9,384 families (M 302, SD 1,052). Studies varied in the extent to which they described the sociodemographic characteristics of families, including marital status, socioeconomic status, racial composition of samples, and the biological status of parents. A total of 444 effect sizes were calculated from these studies. For details of studies, see the Appendix.4

Information Extracted
Studies were coded by a team of three coders, two undergraduates research assistants and Arin M. Connell. Coders were trained to an acceptable level of reliability, and all coded a common subset of 20 articles. Weekly meetings were held to discuss coding and to establish reliability; differences were resolved through discussion. High interrater reliability was found between Arin M. Connell and each of the research assistants, with Cohens kappa ranging from .70 to .80 for sample type, from .70 to 1.00 for method of assessing parents mental health problems, and equal to .90 for both raters for approaches to assessing childrens mental health problems. For all other coding, Cohens kappa was 1.00. Childrens internalizing behavior problems. In total, 230 effect sizes were calculated for the relation between parental mental health problems and childrens internalizing problems. Internalizing behavior problems were coded to indicate whether they were based on symptom ratings or on diagnostic classifications. Studies that used symptom ratings were coded to indicate whether ratings were based on parent report, child report, teacher report, or on combined ratings from multiple informants. Symptom ratings included measures of depressed mood, anxiety, or social withdrawal. Childhood depression and anxiety disorders were included among the measures of diagnostically based studies; the informant for diagnostic assessments was coded to indicate whether diagnoses were based on childrens self-report, parental reports, a review of medical records, or a combination of these assessment methods. If multiple symptom ratings were used, we averaged these together. Similarly, if multiple internalizing diagnoses were examined (e.g., depression and anxiety), these were averaged. If studies used both symptom ratings and diagnoses, these were kept as separate effect sizes. Childrens externalizing behavior problems. In total, 214 effect sizes for the relation between parental mental health problems and childrens externalizing problems were calculated. As with internalizing problems, externalizing problems were first coded to indicate whether they were based on symptom ratings or on diagnostic classifications. We used the same coding scheme for studies that used symptom ratings described for internalizing problems to indicate the source of the ratings. Symptom ratings included measures of aggression, conduct problems, and delinquency. For diagnostically based studies, we used the same coding scheme described for internalizing problems to indicate the informant used. Externalizing diagnoses included CD, ODD, and ADHD. Parental mental health problems. Studies were first coded to reflect the manner in which parental mental health problems were assessed, that is, with either a categorical or dimensional approach to assessment. Next, studies were grouped into larger categories to examine moderation by the type of parental mental health problem. Parental mental health problems

Method Selection of Studies

We used several approaches to locate studies for inclusion in the metaanalysis. The principal method of location involved a search of computerized databases, including PsycINFO and ERIC (collectively covering 1888 2001), for studies presenting quantitative data on the association between parental mental health and child internalizing or externalizing behavior problems. All combinations of key words in the following groupings were used: (a) mother, maternal, mom, father, paternal, dad, parent(al); (b) child(ren), toddler, boy, girl, adolescent; (c) behavior problems, internalizing, depression, anxiety, withdrawn, shy, inhibit(ion), overcontrol, externalizing, conduct disorder, oppositional, delinquent, hyperactive, attention deficit, aggressive, alcohol(ic), alcohol abuse, substance abuse, antisocial, mental health problem, psychopathology. Second, the ancestry method was used, in which references listed in review articles (e.g., Phares & Compas, 1992) or empirical articles were retrieved. Third, a letter was sent to the principal author of the studies identified by the first two methods requesting copies of any relevant unpublished manuscripts or in-press articles. Finally, notices were sent to several Internet-based discussion lists for psychologists requesting copies of any relevant unpublished manuscripts or in-press articles. Though it is likely that other relevant studies exist that were not identified, the scope of the search makes it likely that these studies are at least a representative sample of the total body of potentially available research.

Inclusion Criteria
To be included in the meta-analysis, a study had to meet the following criteria. First, the study had to include separate data on mental health of mothers and fathers. We excluded studies that failed to consider mothers and fathers separately (i.e., included data on parents only). Second, only studies covering the developmental span from toddlerhood through adolescence (roughly ages 218 years) were examined. Studies focusing on retrospective reports of childhood were excluded due to their questionable validity, and studies concerning behavior problems during infancy were excluded due to the difficulty of reliably classifying infant behavior problems into the internalizing and externalizing dimensions. Third, the study had to include measures of child internalizing and/or externalizing behavior problems, which we operationally define in the Results section. Studies with data not clearly split into internalizing or externalizing dimensions (i.e., those that only included ratings of total behavior problems without specifying the nature of those problems) were excluded from consideration.2

Study Sample
In total, results from 134 independent samples from studies published or submitted for publication since 1974 met the inclusion criteria.3 Collec-

2 Though there is growing interest in children with comorbid internalizing and externalizing behavior problems (e.g., Wright et al., 1999), it was not possible to look at such co-occurring problems in this meta-analysis because few studies presented data in a manner to permit such an examination. 3 Although studies published prior to 1974 were examined, none met the criteria for inclusion in this meta-analysis. 4 A more detailed version of the Appendix, including information on each effect size, is available from Sherryl H. Goodman.

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CONNELL AND GOODMAN and provided no statistics to permit the calculation of an exact effect size, we adopted the conservative strategy of assigning a correlation of .00. Effect sizes assessing the same construct within each study were averaged using Fischers r-to-z transformation. We calculated separate average effect sizes for maternal and paternal mental health problems and internalizing and externalizing behavior problems for any of the six parental disorder categories included within each study and, when possible, for boys and for girls. Studies that reported results on multiple subsamples, such as for older and younger children were treated as separate studies. In addition, an a priori decision was made to use only Time 1 results in the case of longitudinal studies. Next, we analyzed data across studies, with the goal of estimating the population effect size and variables that may moderate the strength of the effect sizes across studies. One assumption of the analyses at this stage was that the effect sizes were independentthat is, that each study only contributed one effect size to each analysis. In accordance with the recommendations of Light and Pillemer (1984), independence of effect sizes was emphasized at two levels, first at the study level, with each study allowed to contribute only one effect size to the analyses, and second at the construct level, with each study allowed to contribute one effect size at each level of the moderator variables. Analyses were conducted at each level. The goals of the study-level analyses were to obtain an unbiased estimate of the population effect size and to examine the homogeneity of effect sizes within each of these analyses. For the association between parental mental health problems and child behavior problems, we conducted separate study-level analyses of fathers mental health and child internalizing and externalizing problems and of mothers mental health and child internalizing and externalizing problems, for a total of four analyses. We estimated the population effect size for these analyses by the average effect size (r), with each effect size weighted by its sample size because studies with larger sample sizes should provide a better approximation of the population effect size than smaller studies. The resulting population effect sizes have been interpreted using Cohens (1988) recommendations that an r of at least .10 be termed a small effect, an r of at least .24 be termed a medium effect, and an r of at least .37 be termed a large effect. At the study level, the homogeneity estimate (Q) follows a chi-square distribution and examines the likelihood that the variation in effect sizes within each analysis is different from that which would be expected to result simply from sampling error. A significant homogeneity estimate indicates heterogeneity of effect sizes, such that a moderator search is warranted. In addition, Rosenthals (1991) fail-safe N was calculated at the study level, indicating the number of additional studies with null results that would have to be found in order to bring the mean effect size to zero. The goal of the construct-level analyses was to examine potential moderators of the relations between psychopathology in mothers or fathers and the presence of emotional or behavioral problems in children. We conducted two types of moderator analyses, using procedures described by Cooper and Hedges (1994). For categorical moderating variables, including child gender, type of parental mental health problem, sample type, diagnostic versus symptom rating-based assessment of parents and children, informant for parent and child diagnoses, rater for child symptoms, familial composition, and the biological status of parents, we used categorical model testing procedures. These procedures are analogous to an analysis of variance (ANOVA), with effect sizes grouped according to the levels of the moderator variable. These groups are compared to examine whether they differ significantly from one another. Categorical model testing yields two homogeneity estimates, a between-groups Q (Qb) and a within-groups Q (Qw). A significant Qb indicates that the subgroups of effect sizes are significantly different from one another, and that follow-up contrasts may be conducted to identify which groups differ significantly from one another. A significant Qw indicates that the smaller group of effect sizes is not homogeneous and that substantial variability among the effect sizes is still present. If an analysis yields a significant Qb but the

were grouped into one of seven categories: (a) alcohol or substance abuse or dependence, (b) depression, (c) anxiety disorders, (d) schizophrenia, (e) ASPD, (f) bipolar disorder, and (g) a mixed category, covering those studies that used only a general symptom rating of mental distress. For diagnostically based studies, effects were coded to indicate whether the diagnosis was based on information collected from self-report during a direct interview, spousal report, a review of medical records, or a combination of these assessment methods. Child gender. When possible, we calculated separate effect sizes for boys and girls. When studies did not provide enough information to permit such calculations, child gender was coded as mixed. Only 38 studies provided enough information to permit the calculation of separate effect sizes for boys and girls. Sample type. Sample type was coded on the basis of the recruitment method used. Studies were coded as representing parent clinical samples when study participants were recruited from a clinical setting in which parents were seeking or receiving services for themselves. Studies were coded as representing child clinical samples when study participants were recruited from a clinical setting in which children were referred for or were receiving services. Studies were coded as representing community samples when all participants were recruited from the general community. In total, 28 studies used parent clinical samples, 39 used child clinical samples, and 67 used community samples. Biological status of parents. If studies provided separate effects for biological parents, these effects were coded as representing biological parents. If no information was provided on the biological status of parents or if studies combined biological and nonbiological parents, these effects were coded as not providing information on the biological status of parents. Only seven studies specified the biological status of parents. Family composition. Because very few studies provided separate analyses for intact versus nonintact families, we calculated the percentage of intact families in samples only when such information was provided. The percentages of intact families were highly skewed, with the majority of samples comprised mostly or entirely of intact families, thus a decision was made to examine this moderator categorically. Categories were selected to ensure subgroups of studies large enough to permit meaningful analyses. Four categories were coded. Studies for which no information was provided on the number of intact families in the sample were coded as no information. Samples with fewer than 50% intact families in samples were grouped together, as were samples with 50 99% intact families and studies including only intact families. In total, 65 studies provided no information on family composition, 9 studies examined samples with fewer than 50% intact families, 42 studies examined samples with 50 99% intact families, and 18 studies included only intact families. Child age. The mean age of the children studied in each sample was coded. The mean age of the children in these studies ranged from 1.70 to 17.50 years, with an overall mean of 9.37 years (SD 3.97 years). Year of publication. The year of publication, submission for publication, or conference presentation was coded.

Meta-Analytic Method
Meta-analytic procedures allow researchers to estimate the population effect size of the association between two variables and to search for theoretically or methodologically relevant variables that may moderate the strength of that effect. Following the recommendations of Rosenthal (1994), we decided to use the effect size r in the present study because of its greater familiarity to most readers and because of its conceptual superiority over effect size d in studies involving multiple groups or withingroup designs. Within each study, we calculated effect sizes for each relevant statistical test reported and, when possible, for each level of the moderator variables described above. Effect sizes were calculated using a variety of widely available formulas (see Rosenthal, 1994, for a complete listing). When researchers stated only that no significant effects were found

PATERNAL VERSUS MATERNAL PSYCHOPATHOLOGY subgroups of effects are not homogeneous, follow-up contrasts should be interpreted with caution because there is still substantial variability within the subgroups of effects. To ensure adequate power for follow-up analyses, we performed contrasts only if subgroups were composed of five or more studies. Following procedures described by Hedges (1994), we calculated standardized contrasts (g) from the difference of effect sizes, and we examined the significance of the contrast by dividing it by the pooled variance and comparing the resulting value with the critical value of the chi-square distribution ( p .05). For categorical analyses in which results were predicted to differ for mothers and fathers (i.e., child gender, the type of parental mental health problem, the informant for parental diagnoses, and familial composition), we examined subgroups of effects separately for mothers and fathers, and we conducted follow-up contrasts comparing the magnitude of the effect sizes for mothers and fathers within each level of the moderating variable. For analyses in which mother versus father differences were not predicted (i.e., the use of diagnoses vs. symptom ratings for parents or children, the informant for child diagnoses, the rater for child symptoms, sample type, and the biological status of parents), subgroups of effects combined mothers and fathers, and follow-up contrasts examined differences across these combined subgroups. For continuous moderator variables, including child age and the year of publication, we used weighted least squares regression procedures, as described by Hedges (1994), with effect sizes weighted by the inverse of the variance (which is estimated from sample size). We used simple linear regression procedures to examine whether a significant relationship existed between the value of the moderating variables and the magnitude of the effect size. For each analysis, only one moderator variable was entered into the regression equation, and the resulting correlation is interpreted as usual, with the z test representing a two-sided test of the null hypothesis that the regression coefficient equals zero. Finally, we conducted analyses to examine possible interrelations among moderator variables that may have confounded the results of the moderator analyses. We conducted separate multiple regression analyses for internalizing and externalizing disorders to examine the unique effects of variables that were found to be significantly interrelated.

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ternal mental health problems and child internalizing behavior problems are shown in Table 1. The distributions of the effect sizes for parental mental health problems are shown in Table 2. For the association between mental health problems in fathers and child internalizing problems, the weighted mean effect size was .14, and for mothers the weighted mean effect size was .18. Both population effect sizes were small in magnitude, accounting for less than 5% of the variance in childrens internalizing problems. In addition, both analyses yielded results that were significantly heterogeneous, indicating the likely presence of moderating variables. In a follow-up contrast, a stronger association was found between mothers than fathers mental health problems and childrens internalizing behavior problems (g 0.04, p .05). Though statistically significant, the difference between these average effect sizes was small. Childrens externalizing behavior problems. Results of the study-level analyses for the association between paternal and maternal mental health problems and child externalizing behavior problems are shown in Table 1. The distributions of the effect sizes for parental mental health problems are shown in Table 3. For mothers, the weighted mean effect size was .17, and for fathers the weighted mean effect size was .16. Both results represent small population effect sizes, and both analyses yielded results that were significantly heterogeneous, indicating the likely presence of moderating variables. The weighted mean effect sizes for mothers and fathers were not found to be significantly different from one another in a follow-up contrast (g 0.01, p .05).

Construct-Level Moderator Analyses for Categorical Variables

To examine the possibility that the number of effect sizes contributed by each study to the construct-level moderator analyses would bias the results in favor of studies contributing multiple effect sizes, the number of effect sizes from each study was correlated with the magnitude of the effect sizes. Results were significant but of small magnitude (r .12, p .05), indicating that the construct-level analyses may yield slightly conservative results. Childrens internalizing behavior problems. Results of the construct-level categorical moderator analyses are shown in Table 4. Nine of the 10 analyses found significant between-groups homogeneity, indicating significant differences across subgroups of effects. We conducted follow-up contrasts for these analyses.

Results Study-Level Analyses

For all of the following, meta-analytic reporting conventions were followed, such that at the study level, k represents the number of studies in an analysis and n represents the total number of participants in those studies. For construct-level analyses, k represents the number of effect sizes contributing to an analysis. Childrens internalizing behavior problems. Results of the study-level analyses for the association between paternal and ma-

Table 1 Results of Study-Level Analyses for Child Internalizing and Externalizing Behavior Problems and Parental Mental Health Problems
Child problem Internalizing Externalizing Parent Mother Father Mother Father k 94 59 90 56 n 38,839 25,186 27,199 14,729 Weighted mean r .18a .14a .17 .16 95% CI .17.19 .13.15 .16.18 .15.18 Q 329.85*** 207.57*** 331.11*** 172.40*** Fail-safe N 238 104 216 129 studies studies studies studies

Note. Matching subscripts indicate significant differences. k the number of studies in an analysis; n the total number of participants in those studies; CI confidence interval; Q homogeneity estimate. *** p .001.

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Table 2 Stem and Leaf Display of Effect Sizes for the Association Between Parental Mental Health Problems and Externalizing Behavior Problems in Children
Stem Leaf Fathers mental health problems .9 .8 .7 .6 .5 .4 .3 .2 .1 .0 .0 .1 .2 .3 .4 .5 .6 .7 .8 .9

anxiety, ASPD, schizophrenia, bipolar disorder, or general symptoms for mothers and fathers), 3 of the 13 groups were found to be homogeneous, although only 1 of these groups contained more than five effect sizes. Three of the weighted mean effect sizes were not significantly different from zero: bipolar disorder in mothers and ASPD and schizophrenia in fathers. Follow-up contrasts compared the strength of effect sizes for each disorder in mothers versus fathers. Only one contrast was significant, with depression in mothers more strongly related to childrens internalizing problems than depression in fathers (g 0.02, p .05). We did not perform contrasts for ASPD, schizophrenia, or bipolar disorder because subgroups for one or both parents had fewer than five studies.

2 0, 0, 0, 0, 0, 2, 1, 0

0, 0, 2, 0, 2, 6, 4,

0, 0, 3, 0, 3, 9 8

1 1, 4, 0, 4,

5, 6, 7, 7, 8 5, 6, 7, 8, 8, 9, 9 1, 1, 1, 3, 4, 4, 7, 8 6

Table 3 Stem and Leaf Display of Effect Sizes for the Association Between Parental Mental Health Problems and Internalizing Behavior Problems in Children
Stem Leaf Fathers mental health problems .9 .8 .7 .6 .5 .4 .3 .2 .1 .0 .0 .1 .2 .3 .4 .5 .6 .7 .8 .9

Mothers mental health problems .9 .8 .7 .6 .5 .4 .3 .2 .1 .0 .0 .1 .2 .3 .4 .5 .6 .7 .8 .9

0, 0, 0, 0, 0, 0, 0, 3

0, 0, 1, 0, 1, 1, 3,

0, 0, 1, 0, 1, 2, 3,

0, 0, 1, 1, 2, 2, 4,

0 0, 1, 1, 3, 3, 5

2, 2, 2, 8 4,

3, 6, 6, 6, 8, 9, 9 3, 4, 4, 5, 5, 6, 7, 9 2, 2, 3, 3, 3, 7, 7, 7, 7, 8, 8, 9, 9, 9 4, 8

3 0, 0, 0, 0, 1, 0,

0, 0, 1, 0, 3, 1,

4, 3, 1, 1, 3, 2,

7, 4, 2, 1, 6, 2,

8 4, 3, 2, 7, 7,

5, 3, 3, 7, 8

6, 3, 4, 7,

7, 9 5, 6, 7, 8, 8, 9 5, 8, 9 8

Mothers mental health problems .9 .8 .7 .6 .5 .4 .3 .2 .1 .0 .0 .1 .2 .3 .4 .5 .6 .7 .8 .9

However, substantial variability remained for most subgroups in these analyses; therefore, these contrasts should be interpreted with caution. For the analysis examining moderation by childrens gender, two of the six groups were found to be homogeneous, and all weighted mean effect sizes were significantly greater than zero. Follow-up contrasts examined differences between effects for mothers and fathers within each gender. Maternal psychopathology was more strongly related to internalizing problems than paternal psychopathology for boys (g 0.03, p .05), girls (g 0.03, p .05), and for samples combining boys and girls (g 0.03, p .05). In the analysis examining moderation by the type of parental mental health problem (alcoholism or substance abuse, depression,

0, 0, 0, 0, 0, 0, 1, 0

0, 0, 1, 0, 1, 2, 3,

4 1, 1, 1, 2, 3, 4,

2, 2, 1, 3, 4, 4,

4, 4, 1, 4, 4, 6

5, 4, 3, 5, 5,

6, 4, 3, 5, 7,

6, 5, 4, 5, 8,

7, 5, 4, 9 8,

7, 8, 8, 9, 9 5, 6, 6, 6, 7, 8, 9 5, 6, 6, 6, 7, 7, 7, 7, 8, 9, 9, 9 8

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Although the analysis examining moderation by the use of parental diagnoses versus symptom ratings indicated that studies using symptom ratings for parents tended to yield larger effects than studies using diagnoses for parents, neither subgroup was homogeneous. As such, this difference should be interpreted with caution. For the analysis examining moderation by the informant for parental diagnoses, four of eight groups were found to be homogeneous, although one of these groups consisted of fewer than five studies. Because no studies relied on spouse reports for maternal psychopathology and fewer than five studies relied on spouses as informants for paternal psychopathology, no follow-up analyses were examined for this group. Furthermore, because we had predicted no motherfather differences for the remaining groups, follow-up contrasts examined differences across informants for mothers and fathers combined. Studies relying on direct interviews of parents found larger effects than studies relying on either medical records (g 0.16, p .05) or multiple informants (g 0.15, p .05). Effects from these latter two groups did not differ from one another (g 0.01, p .05). Although the analysis examining moderation by the use of child diagnoses versus symptom ratings indicated that studies using symptom ratings for children tended to yield larger effects than studies using diagnoses, neither subgroup was homogeneous. As such, this difference should be interpreted with caution. For the analysis examining moderation of effect sizes by the source of the rating of childrens internalizing symptoms (child, parent, or teacher ratings for mothers and fathers), only one subgroup demonstrated within-group homogeneity; therefore, follow-up contrasts should be interpreted cautiously. In follow-up contrasts, studies exclusively using parent ratings were found to yield significantly larger effects than studies using either child ratings (g 0.22, p .05) or teacher ratings (g 0.36, p .05) but to not yield significantly larger effects than studies combining ratings from different sources (g 0.02, p .05). Similarly, results from studies combining ratings from multiple raters found larger effects than studies relying on child ratings (g 0.07, p .05) or teacher ratings (g 0.20, p .05). In turn, studies relying on childrens ratings of their own symptoms found significantly larger effects than studies relying on teachers ratings of childrens internalizing symptoms (g 0.13, p .05). For the analysis examining moderation by the informant for childrens diagnoses, only one group demonstrated within-group homogeneity; therefore follow-up contrasts should be interpreted with caution. In follow-up contrasts, studies combining information from multiple informants for child diagnoses were found to yield larger effects than studies relying on parents (g 0.06, p .05) or on medical records for diagnostic information (g 0.10, p .05). Similarly, studies relying on children for diagnostic information yielded larger effects than studies relying on medical records (g 0.08, p .05). No other follow-up contrasts achieved significance. For the analysis examining moderation of effect sizes by the type of sample used, none of the three subgroups demonstrated within-group homogeneity. Thus, follow-up contrasts should be interpreted with caution. Such contrasts indicated that studies using samples of clinic-referred parents yielded larger effects than studies using samples of clinic-referred children (g 0.06, p

.05) or community-based samples (g 0.07, p .05). These latter two groups did not differ significantly from one another. For the analysis examining moderation of effect sizes by the composition of families within the samples, three of the eight groups demonstrated within-group homogeneity, although one of these groups consisted of fewer than five effects. Our follow-up analyses examined differences across the three groups of family composition separately for mothers and fathers because we had predicted that patterns would differ between mothers and fathers across different family compositions. We did not conduct follow-up analyses on the group of studies that provided no information on family composition because we had made no predictions for such studies and because results of such analyses would be difficult to substantively interpret. For mothers, samples composed entirely of intact families yielded larger effects than samples with 50 99% intact families (g 0.08, p .05). For fathers, only four studies had samples with fewer than 50% intact families; therefore, we did not examine follow-up contrasts for this group. As was the case for mothers, effects from samples with 100% intact families were significantly larger than those with 50 99% intact families (g 0.13, p .05). The analysis examining moderation of effect sizes by the biological status of parents found no significant difference between effects from studies using only biological parents and those either combining biological and nonbiological parents or providing no information on parents biological status. Childrens externalizing behavior problems. Results for the categorical moderator analyses are shown in Table 5. Eight of the 10 analyses found significant between-groups homogeneity, indicating significant differences across subgroups of effects. We conducted follow-up contrasts for these analyses. However, substantial variability remained for most subgroups in these analyses; therefore, these contrasts should be interpreted with caution. For the analysis examining moderation by childrens gender, none of the subgroups were found to be homogeneous. Thus, these follow-up contrasts should be interpreted with caution. We performed follow-up contrasts to examine differences between effects for mothers and fathers within each gender. Paternal psychopathology was more strongly related to externalizing problems than maternal psychopathology for girls (g 0.06, p .05), whereas maternal psychopathology was more strongly related to externalizing problems in samples combining boys and girls than paternal psychopathology (g 0.02, p .05). In the analysis examining moderation by the type of parental mental health problem, 4 of the 14 groups demonstrated withingroup homogeneity, although 3 of these groups consisted of fewer than five studies. Furthermore, an additional subgroup examining paternal schizophrenia consisted of only one study. Five of the mean effect sizes were not significantly different from zero; maternal and paternal schizophrenia, maternal and paternal bipolar affective disorder, and paternal anxiety were not significantly related to childrens externalizing behavior problems. Follow-up contrasts compared the strength of effect sizes for each disorder in mothers versus fathers. Only one such contrast was significant, with maternal alcoholism more strongly related to childrens externalizing problems than paternal alcoholism (g 0.04, p .05). We did not perform contrasts for anxiety disorders, schizophrenia, or bipolar disorder because these groups had fewer than five studies for one or both parents.

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Table 4 Moderator Analyses for Child Internalizing Behavior and Parental Mental Health Problems
Level of moderator Child gender Mother Boy Girl Mixed Father Boy Girl Mixed Parental mental health problem Mother Alcohol or substance abuse Depression Anxiety ASPD Schizophrenia Bipolar Mixed Father Alcohol or substance abuse Depression Anxiety ASPD Schizophrenia Mixed Parent diagnosis vs. symptom rating Parent diagnosis Parent symptom rating Informant for parental diagnoses Mother Self Spouse Chart review Combined Father Self Spouse Chart review Combined Child diagnosis vs. symptom rating Child diagnosis Child symptom rating Rater for child symptoms Child Parent Teacher Combined Informant for child diagnoses Child Parent Chart review Combined Sample type Parent clinical Child clinical Community Percentage of two-parent families Mother No information 50% 5099% 100% Qb 19.20** 15 15 115 19 15 51 41.85*** 14 78 25 4 6 4 14 29 31 8 4 3 10 28.98*** 112 118 47.08*** 53 0 5 7 40 4 3 6 6.80** 88 142 101.13*** 35 68 8 17 10.55* 38 17 10 23 15.47** 41 74 115 54.67*** 68 7 54 16 .15 .19 .16a .24a .14.16 .12.26 .15.18 .20.28 244.99*** 13.35 123.42*** 41.04*** .21a,b .15a .14b .18.24 .14.16 .13.15 78.70*** 166.43*** 409.66*** .14a .10b .07a,c .16b,c .11.17 .06.15 .02.12 .12.20 69.47** 44.56*** 4.05 39.92* .14a,b,c .23a,d .01b,d,e .21c,e .13.15 .21.26 .04.06 .18.24 124.97*** 182.65*** 23.56** 16.54 .13a .15a .11.15 .15.16 168.55*** 494.89*** .14a,b .10a .06b .16a,b .04 .04a .09b .12.15 .04.17 .01.13 .13.19 .10.02 .05.13 .01.17 193.12*** 4.57 7.14 98.00*** 12.61* 0.49 3.18 .13a .17a .11.14 .16.18 351.75*** 289.52*** .11 .16a .16 .10 .11 .03 .19 .12 .14a .13 .05 .02 .14 .06.15 .15.17 .14.18 .05.15 .04.17 .09.15 .15.22 .08.15 .12.16 .07.20 .04.15 .07.11 .10.18 26.61** 255.64*** 51.75** 21.71* 21.84** 15.28** 32.95** 95.28*** 79.29*** 1.86 4.70 0.23 28.27** .17a .17b .15c .14a .14b .12c .15.19 .15.19 .14.16 .12.16 .11.16 .10.14 23.60 23.37 386.71*** 87.70*** 45.00*** 84.74** k Weighted mean r 95% CI Qw

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Table 4 (continued )
Level of moderator Percentage of two-parent families (continued) Father No information 50% 5099% 100% Biological parents vs. no information Biological No information Qb k Weighted mean r 95% CI Qw

37 4 23 21 0.30 10 220

.13 .27 .08b .21b .16 .15

.12.14 .13.42 .05.12 .17.25 .12.21 .14.16

111.12*** 2.63 58.57*** 20.46 0.74 666.70***

Note. Matching subscripts indicate significant differences. Qb between-groups homogeneity estimate; k the numbers of studies in an analysis; CI confidence interval; Qw within-group homogeneity estimate; ASPD antisocial personality disorder. * p .05. ** p .01. *** p .001.

We conducted an analysis to examine the moderation of effect sizes by the method of assessing parental psychopathology. This analysis found no significant difference between effects from studies using diagnoses versus symptom ratings of parental psychopathology. For the analysis examining moderation by the informant for parental diagnoses, four of six groups were found to be homogeneous, although two of these groups consisted of fewer than five studies. For mothers, no studies relied on spouse reports or combined information from multiple informants. Although no mother father differences were predicted for this moderator, the absence of effects for two of the maternal subgroups prevented combining mothers and fathers for follow-up analyses; therefore, we conducted separate follow-up contrasts for mothers and fathers to examine differences across informants. However, because fewer than five studies relied on chart reviews for maternal diagnoses, no follow-up analyses were conducted for mothers. Similarly, because fewer than five studies relied on chart reviews for paternal diagnoses, no follow-up contrasts were conducted for this subgroup. Studies relying on direct interviews of fathers yielded larger effects than studies relying on either indirect reports from wives or on a combination of information from multiple informants (selfreportspouse report: g 0.08, p .05; self-reportmultiple informants: g 0.19, p .05). Furthermore, studies relying on wives reports of their husbands mental health yielded larger effects than studies combining information from multiple informants (g 0.11, p .05). Although the analysis examining moderation by the use of child diagnoses versus symptom ratings indicates that studies using symptom ratings for children yielded larger effects than studies using diagnoses, neither subgroup was homogeneous. As such, this difference should be interpreted with caution. For the analysis examining moderation of effect sizes by the source of the rating of childrens externalizing symptoms, no subgroup demonstrated within-group homogeneity; therefore, follow-up contrasts should be interpreted cautiously. In follow-up contrasts, studies exclusively using parent ratings were found to yield significantly larger effects than studies using either child ratings (g 0.10, p .05), teacher ratings (g 0.07, p .05), or combined ratings from multiple sources (g 0.05 p .05). In turn,

results from studies using combined ratings from multiple raters were larger than those from studies relying on child ratings (g 0.05, p .05). For the analysis examining moderation by the informant for childrens externalizing diagnoses, two of four groups were homogeneous, although one of these consisted of fewer than five cases. Because fewer than five studies relied on medical records for childrens diagnoses, we examined no follow-up contrasts for this group. In the follow-up contrasts, studies using children as informants yielded larger effects than studies relying on multiple informants (g 0.07, p .05) or on parents as informants (g 0.12, p .05). In turn, studies relying on multiple informants found larger effects than studies relying on parental reports (g 0.05, p .05). The analysis examining moderation of effect sizes by the type of sample used found no significant variation across groups of effects on the basis of use of parent clinical, child clinical, or community samples. For the analysis examining moderation of effect sizes by the composition of families within the samples, only one subgroup (consisting of fewer than five effects) demonstrated within-group homogeneity; therefore, follow-up contrasts should be interpreted with caution. Follow-up analyses examined differences across the three groups of family composition separately for mothers and fathers because we had predicted that patterns would differ between mothers and fathers across different family compositions. We did not conduct follow-up analyses on the group of studies that provided no information on family composition because no predictions were made for such studies and because results of analyses concerning this group would be difficult to substantively interpret. For mothers, follow-up contrasts revealed that samples with 100% intact families yielded larger effects than samples with 50 99% intact families (g 0.08, p .05). Similarly, samples composed of fewer than 50% intact families yielded larger effects than samples with 50 99% intact families (g 0.09, p .05). For fathers, only three studies had samples with fewer than 50% intact families; therefore, we did not examine follow-up contrasts for this group. As for mothers, effects from samples with 100% intact families were significantly larger than those with 50 99% intact families (g 0.12, p .05).

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Table 5 Moderator Analyses for Child Externalizing Behavior and Parental Mental Health Problems
Level of moderator Child gender Mother Boy Girl Mixed Father Boy Girl Mixed Type of Parental mental health problem Mother Alcohol or substance abuse Depression Anxiety ASPD Schizophrenia Bipolar Mixed Father Alcohol or substance abuse Depression Anxiety ASPD Schizophrenia Bipolar Mixed Parent diagnosis vs. symptom rating Parent diagnosis Parent symptom rating Informant for parental diagnoses Mother Self Spouse Chart review Combined Father Self Spouse Chart review Combined Child diagnosis vs. symptom rating Child diagnosis Child symptom rating Rater for child symptoms Child Parent Teacher Combined Informant for child diagnoses Child Parent Chart Review Combined Sample type Parent clinical Child clinical Community Percentage of two-parent families Mother No information 50% 5099% 100% Qb 12.61* 35 14 84 35 12 34 79.36*** 13 79 9 10 3 6 13 32 26 2 9 1 2 9 1.65 108 106 45.19*** 53 0 2 0 38 5 3 9 7.69** 74 140 94.27*** 11 75 12 21 14.25** 7 28 2 47 5.89 34 79 101 72.90*** 68 9 44 12 .12 .26a .17a,b .25b .11.14 .20.33 .15.18 .20.30 193.56*** 17.09* 111.54*** 38.38*** .18 .13 .15 .14.21 .11.15 .14.16 89.95*** 205.11*** 347.53*** .19a,b .07a,c .22 .12b,c .14.25 .04.11 .02.42 .09.14 3.89 47.15* 4.31 135.58*** .11a,b .21a,c,d .14c .16b,d .09.12 .20.23 .10.18 .14.18 25.76** 208.73*** 23.43* 35.17* .12a .15a .10.14 .14.16 177.42*** 463.38*** .13 .23 .19a,b .11a,c .25 .00b,c .12.15 .11.36 .16.21 .06.16 .16.34 .07.07 193.14*** 3.10 103.18*** 6.77 5.53 14.39 .14 .15 .13.15 .14.17 367.77*** 279.07*** .20a .14 .13 .13 .06 .01 .19 .16a .10 .07 .19 .00 .13 .18 .18.22 .13.15 .11.15 .09.17 .03.15 .08.10 .16.23 .14.18 .06.13 .03.16 .14.25 .11.11 .27.01 .13.22 42.88*** 223.90*** 4.32 23.51** 0.41 15.30* 58.50*** 87.66*** 53.44** 2.69 18.23* 0.00 0.12 38.18*** .13 .16a .15b .16 .22a .13b .10.16 .12.20 .14.16 .13.18 .16.27 .11.15 79.80*** 30.96** 296.77*** 74.94*** 57.27*** 96.15*** k Weighted mean r 95% CI Qw

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Table 5 (continued )
Level of moderator Percentage of two-parent families (continued) Father No information 50% 5099% 100% Biological parents vs. no information Biological No information Qb k Weighted mean r 95% CI Qw

40 3 21 17 4.10* 26 188

.15 .16 .11c .23c .11a .15a

.13.18 .01.30 .08.13 .19.27 .08.15 .14.16

130.22*** 2.76 45.85** 34.19** 68.82*** 575.58***

Note. Matching subscripts indicate significant differences. Qb between-groups homogeneity estimate; k the number of studies in an analysis; CI confidence interval; Qw within-group homogeneity estimate; ASPD antisocial personality disorder. * p .05. ** p .01. *** p .001.

The analysis examining moderation by the biological status of parents revealed that studies using biological parents tended to find smaller results than studies either combining biological and nonbiological parents or not specifying parental status. However, because neither subgroup was found to be homogeneous, this difference should be interpreted with caution.

Moderator Analyses for Continuous Moderator Variables

We conducted a series of weighted least squares regression analyses to examine whether the year of publication or the mean age of children in the samples were significantly related to the magnitude of effect sizes. Results for these analyses are shown in Table 6. Year of publication was significantly related to the magnitude of effect sizes for the association between maternal psychopathology and childrens internalizing and externalizing problems and paternal psychopathology and childrens externalizing problems. Studies published more recently found smaller effect sizes. The mean age of children in the samples was significantly related to the magnitude of effect sizes for the relations between both maternal and paternal psychopathology and childrens internalizing and externalizing behavior problems. A contrasting pattern of age effects was found for mothers versus fathers. For

Table 6 Correlations Between Year of Publication and the Mean Age of Children Studied With Effect Size for Parental Psychological Symptoms and Child Behavior Problems
Child problem Internalizing Mother (k 133) Father (k 86) Externalizing Mother (k 111) Father (k 82) Year of publication (r) .11* .06 .25* .10* Child age (r) .15* .34* .19* .23*

Note. k the number of studies in an analysis. * p .05.

mothers, smaller effects were found in samples of older children. For fathers, however, larger effects were found in studies examining internalizing and externalizing problems in older children. To examine these contrasting age effects for mothers and fathers in more detail, we conducted two sets of follow-up analyses. First, to more directly compare maternal versus paternal effects for children of different ages, studies were grouped according to the mean age of children studied into one of three age ranges: (a) early childhood (mean age 6 years), (b) middle childhood (mean age range 6 13 years), and (c) adolescence (mean age 13). Results of these analyses are shown in Table 7. For internalizing problems, significant differences for maternal versus paternal psychopathology were found within each of these three age ranges. In the early and middle childhood groups, effects for maternal psychopathology were significantly larger than those for paternal psychopathology (early childhood: g 0.10, p .05; middle childhood: g 0.04, p .05). For the adolescence group, conversely, effects for paternal psychopathology were significantly larger than effects for maternal psychopathology (g 0.10, p .05). A similar pattern of maternal versus paternal differences was found for externalizing problems, although effects for maternal and paternal psychopathology did not differ in middle childhood. In the early childhood group, effects for maternal psychopathology were found to be significantly larger than those for paternal psychopathology (g 0.09, p .05), whereas in the adolescence group, effects for paternal psychopathology were found to be significantly larger than those for maternal psychopathology (g 0.10, p .05). Second, to determine whether these age effects would be found for different parental disorders, we conducted a series of more detailed regression analyses that examined age trends for separate diagnoses. An a priori decision was made to conduct analyses only for groups of effects containing more than 10 effect sizes, in an attempt to ensure a large enough distribution to yield meaningful results. As shown in Table 8, 12 analyses were conducted. For mothers, the pattern of finding smaller effects in samples studying older children was found in two of the analyses. However, the direction of the association was reversed for studies examining the relation between maternal alcoholism and childrens externalizing

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Table 7 Follow-Up Analyses for Childrens Age as Moderator

Age range Internalizing Mother 6 613 13 Father 6 613 13 Externalizing Mother 6 613 13 Father 6 613 13 Qb 41.03*** 26 85 22 10 62 14 51.74*** 30 64 17 13 55 14 .16a .17 .12b .07a .16 .22b .13.20 .17.20 .11.13 .02.11 .14.18 .15.21 76.75*** 106.61*** 105.71*** 17.73 99.99*** 96.88*** .19a .17b .13c .09a .13b .23c .14.23 .16.18 .12.14 .04.15 .12.14 .18.29 66.36*** 197.11*** 107.86*** 17.26 165.73*** 20.58 k Weighted mean r 95% CI Qw

Note. Matching subscripts indicate significant differences. Qb between-groups homogeneity estimate; k the number of studies in an analysis; CI confidence interval; Qw within-group homogeneity estimate. * p .05. ** p .01. *** p .001.

problems, with larger effects found in studies examining older children. For fathers, the pattern of finding larger effects in samples studying older children was found in three of the five analyses.

Similarly, we conducted a series of 20 one-way ANOVAs to examine whether the year of study publication differed significantly across subgroups for the 10 categorical moderators. We conducted separate analyses for internalizing and externalizing problems in children. As we stated, 1 analysis out of 20 would be expected to achieve significance by chance. For internalizing problems, 3 of 10 analyses revealed significant differences. First, results revealed that the year of study publication differed by sample type, F(1, 229) 29.03, p .05, as studies using child clinical samples were generally published earlier (M 1987, SD 7.50) than studies using either parent clinical (M 1992, SD 5.68) or community samples (M 1994, SD 4.29). Second, the year of study publication differed by the method of assessing mental health problems in parents, F(1, 229) 5.21, p .05, with studies using parental diagnoses generally published earlier (M 1990, SD 7.01) than studies using symptom ratings for parents (M 1992, SD 5.72). Third, the year of publication differed by the method of assessing childrens internalizing problems, F(1, 229) 20.30, p .05, with studies using child diagnoses generally published earlier (M 1989, SD 6.58) than studies using symptom ratings for children (M 1993, SD 6.58). For externalizing problems, 2 of 10 analyses were significant. First, results revealed that the year of study publication differed by sample type, F(1, 214) 23.51, p .05, with studies using child clinical samples generally published earlier (M 1988, SD 7.10) than parent clinical (M 1992, SD 5.80) or community samples (M 1994, SD 3.92). Second, the year of study publication was related to the method of assessing externalizing problems in children, as studies using child diagnoses were generally published earlier (M 1989, SD 6.35) than studies relying on symptom ratings for children (M 1993, SD 5.67), F(1, 214) 20.39, p .05. Table 8 Correlations Between Mean Age of Children Studied With Effect Sizes for Specific Forms of Parental Psychopathology
Mother Type of parental psychopathology r (k) Child internalizing problems Alcohol or substance abuse Depression Anxiety ASPD Mix Schizophrenia Bipolar disorder .14 (14) .29* (65) .21 (24) (4) .26 (11) (6) (4) .59* (30) .07 (31) (8) (4) .34 (10) (3) (0) Father r (k)

Interrelations Among Moderators

Although the above analyses examined the relations between individual moderators and the magnitude of effect sizes, it is possible that these individual moderators may be related to one another, which may confound the results of the individual analyses. We conducted a series of analyses to examine possible interrelations among the moderator variables. First, a correlational analysis indicated that the continuous variables of the mean age of children studied and the year of study publication were not significantly related to one another (r .04, p .05). Second, we conducted a series of 20 one-way ANOVAs to examine whether the mean age of children studied differed significantly across subgroups for the 10 categorical moderators. Separate analyses were conducted for internalizing and externalizing problems in children. Out of 20 ANOVAs, 1 would be expected to be significant by chance. Only 2 of these 20 analyses revealed significant differences in childrens ages across subgroups. For externalizing problems, studies relying on parental diagnoses included older children (M 10.00, SD 2.89) more often than did studies using symptom ratings of parental mental health problems (M 8.43, SD 4.05), F(1, 214) 10.58, p .05. For internalizing problems, studies relying on child diagnoses included older children (M 10.54, SD 2.85) more often than did studies relying on symptom ratings of childrens problems (M 9.14, SD 3.86), F(1, 229) 8.67, p .05.

Child externalizing problems Alcohol or substance abuse Depression Anxiety ASPD Mix Schizophrenia Bipolar disorder .61* (11) .40* (54) (7) (8) .01 (11) (3) (4) .23* (32) .38* (24) (8) (5) (9) (3) (0)

Note. Dashes indicate too few studies to conduct analyses. k the number of studies in an analysis; ASPD antisocial personality disorder. * p .05.

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We conducted a chi-square analysis to examine whether the method of assessing parents mental health problems (diagnosis vs. symptom rating) was related to the method of assessing problems in children (diagnosis vs. symptom rating). Results revealed that studies tended to use the same approach to assessing parents and children, 2(1, N 444) 77.35, p .05. Studies using a diagnostic approach to assessing parents mental health problems were more likely to use a diagnostic (n 124) than a symptomrating approach (n 96) to assessing childrens internalizing or externalizing problems. Conversely, studies using a symptomrating approach to assessing parents psychopathology were more likely to use a symptom-rating approach to assessing childrens problems (n 38) than a diagnostic approach (n 186). Because the above analyses indicated that several moderator variables were interrelated, we conducted two separate multiple regression analyses for internalizing and externalizing problems to examine the unique contributions of these moderator variables in predicting the magnitude of effects. Only moderators found to be related to other moderators were entered into these analyses. However, because earlier analyses showed that the relation between the age of children studied and the magnitude of effects differed by parent gender, parent gender and the Child Age Parent Gender interaction were entered into these analyses. In addition, because sample type is a three-level variable, we used two effect codes to represent contrasts between the three sample types. The first effect code compares the magnitude of effects from community samples with the magnitude of effects from parent and child clinical samples combined. The second effect code compares the magnitude of parent clinical samples with the magnitude of effects from child clinical samples. Results of these analyses are presented in Table 9. For internalizing problems, the following moderators made significant independent contributions: (a) the mean age of children studied (smaller effects were found for older children), (b) parent gender (effects for mothers were larger than effects for fathers), (c) the method of assessing parents mental

health problems (diagnostically based effects were larger than effects based on symptom ratings), and (d) the Child Age Parent Gender interaction (with the contrasting age effect for mothers vs. fathers discussed previously). For externalizing problems, the following moderators made significant independent contributions to the prediction of the magnitude of effects: (a) parent gender (effects for mothers were larger than effects for fathers), (b) the year of study publication (studies published more recently found smaller effects), (c) the method of assessing childrens externalizing problems (diagnostically based effects were smaller than symptom-based effects), (d) the difference between parent clinical and child clinical samples (parent clinical samples yielded larger effects than child clinical samples), and (e) the Child Age Parent Gender interaction (with the contrasting age effect for mothers vs. fathers discussed previously).

Discussion
The overarching goal of this article was to examine the relative magnitude of association between childrens behavior problems and psychopathology in mothers versus fathers. Although clinical psychology historically has been dominated by an attitude of mother-blaming, researchers and clinicians alike have gradually come to recognize that fathers are an important source of risk for children as well. Although previous reviews (e.g., Phares, 1996; Phares & Compas, 1992) have demonstrated that paternal characteristics are associated with child maladjustment, the magnitude of fathers relative to mothers contributions to this maladjustment has been a matter of disagreement. The results of the study-level analyses indicate that externalizing problems in children were equally related to the presence of psychopathology in mothers and fathers, whereas childrens internalizing problems were more closely related to the presence of psychopathology in mothers than in fathers. However, the magnitude of this difference was small. Furthermore, all of the population effect sizes were of small magnitude, although substantial variability in effect sizes was found in all of these analyses. In light of this variability in effect sizes, results from the moderator analyses qualify these overall conclusions in several important ways. Results of the construct-level moderator analyses indicate that some of the variability in the magnitude of results across studies is related to theoretically relevant differences between the manner in which maternal versus paternal psychopathology is related to the presence of internalizing and externalizing disorders in children. Theoretically relevant moderators include the mean age of children studied and the type of mental health problem in parents. Although theoretically based predictions regarding childrens gender and the year of study publication were posited, they were not supported and therefore are not discussed further. In addition to theoretically relevant differences between mothers and fathers, results of the moderator analyses also indicate that much of the difference in the magnitude of effect sizes across studies appears to be related to methodological differences across studies (rather than to differences between the effects of psychopathology in mothers vs. fathers per se), including the method of assessing mental health problems in parents and children, the type of sample recruited, and family composition. Although a methodologically based prediction regarding the influence of the biological status of parents was posited, it was not generally supported

Table 9 Multiple Regression Analyses for Interrelated Moderator Variables

Variable Child internalizing problems Mean age of children Parent gender Year of study publication Parent diagnosis versus symptom rating Child diagnosis versus symptom rating Community versus parent or child clinical sample Parent clinical versus child clinical sample Mean Age of Children Parent Gender Child externalizing problems Mean age of children Parent gender Year of study publication Parent diagnosis versus symptom rating Child diagnosis versus symptom rating Community versus parent or child clinical sample Parent clinical versus child clinical sample Mean Age of Children Parent Gender * p .05. B 0.58* 1.04* 0.04 0.19* 0.11 0.16 0.25 1.00* 0.40 0.47* 0.26* 0.00 0.19* 0.04 0.10* 0.53*

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and therefore is not discussed further. We now discuss the theoretically and methodologically relevant findings in turn. Foremost among the theoretically relevant findings, the mean age of children studied was found to be related to the magnitude of the association between psychopathology in mothers and fathers and the presence of internalizing and externalizing disorders in children. It is notable that a striking difference in the direction of age effects was found for mothers and fathers, with paternal psychopathology (particularly alcoholism and depression) more closely related to emotional and behavior problems in samples examining older children, whereas maternal psychopathology (particularly depression) was more closely related to emotional and behavioral problems in samples examining younger children. Differences between the direction of age effects for mothers and fathers remained significant with the effects of potentially confounding moderator variables controlled. This pattern of results is generally consistent with our prediction stemming from findings that fathers are more involved in caring for older versus younger children (Bailey, 1994) and may indicate that psychopathology in fathers becomes more salient for children later in development. It may be that mothers are more exclusively important to children during early development because of their role as primary caretaker. Conversely, as caretaking is less often performed by fathers during this early period of development, paternal psychopathology may not have as much of an impact on young childrens social and emotional development but may become increasingly important as children mature and fathers become increasingly salient agents of socialization (Lamb, 1997).5 It is also important to consider the direction of influence in the associations between parental psychopathology and childrens behavior problems in relation to the contrasting pattern of age effects for mothers and fathers. Rather than simply reflecting the causal influence of parental psychopathology on the development of internalizing and externalizing disorders in children, it is likely that the association is bidirectional, as the presence of emotional and behavior problems in children may be a stressor for mothers and fathers, which may affect parents mental health. Several researchers have argued that the nature of childrens behavior problems may change across development such that in young children, displays of emotional and behavior problems may reflect the childs attempts to establish autonomy and instrumentality, whereas in later childhood and adolescence, internalizing and externalizing problems are more reflective of problems with emotion regulation and negative affectivity (Crockenberg & Litman, 1990; Patterson, 1980; Rothbaum & Weisz, 1989, 1994; ZahnWaxler, Iannotti, Cummings, & Denham, 1990). It may be that mothers are more distressed than fathers by the emotional and behavioral outbursts of early childhood. Conversely, fathers may be more distressed than mothers by the withdrawal, irritability, or aggressive acting-out behaviors associated with internalizing or externalizing disorders in adolescence. A qualifier is that this pattern of age effects did not hold for the relation between maternal alcoholism and substance abuse and childrens externalizing problems, for which larger effects were found in samples of older children and adolescents. For this disorder, cumulative exposure may be a critical factor in explaining the larger effects for both maternal and paternal substance abuse and childrens externalizing (and for fathers, internalizing) behavior problems. As alcoholism and substance abuse often fol-

low a chronic course, with increasing severity of incapacitation often accompanying prolonged abuse (e.g., Hasin, VanRossem, McCloud, & Endicott, 1997; Vaillant, 1996), it may be that children are more severely affected by prolonged exposure to this form of parental disorder. A second finding related to theoretically relevant differences between maternal and paternal psychopathology is that differences in the strength of the association between fathers versus mothers psychopathology and internalizing or externalizing problems in children were found for two disorders in parents. First, depression in mothers was found to be more closely related to childrens internalizing (but not externalizing) problems than depression in fathers. Such a difference is consistent with several mechanisms of transmission, including depression-related disruptions to the intrauterine environment during pregnancy and the greater effect of depression on maternal versus paternal parenting (e.g., Field et al., 1999). Second, alcoholism and substance abuse disorders in mothers were more closely related to externalizing (but not internalizing) problems in children than were such disorders in fathers. Although this finding is contrary to the prediction based on a genetic mechanism of transmission, which posited that paternal alcoholism would be more strongly linked to childrens (especially boys) behavior problems, it is consistent with the adverse influence of maternal substance use during pregnancy on prenatal development. For both depression and substance abuse findings, however, the possible role of prenatal influences relating to maternal versus paternal effects remains tentative because most studies did not assess the presence of such disorders during pregnancy. This lack of information highlights the need for researchers to carefully assess parents mental health histories in order to understand the full picture of developmental influences on children. Furthermore, caution is warranted in interpreting the differences between maternal and paternal depression and substance use disorders because the magnitude of the differences were small and because differences for both parental disorders were not found for both internalizing and externalizing disorders in children. Aside from these two disorders, results indicate that the presence of disorder in mothers and fathers generally present equivalent risks for children (although too few studies were available to permit follow-up contrasts for several disorders, including schizophrenia and bipolar affective disorder). However, it bears emphasizing that the prevalence rates of disorders such as depression, anxiety, alcoholism, and ASPD differ in women and men (e.g., Kohn, Dohrenwend, & Mirotznik, 1998). As such, the presence of disorders in women versus men may still reflect differences in
5

Another possible interpretation is that the increase in associations for paternal psychopathology with age are due to the prevalence of some disorders increasing with age. In light of the contrasting pattern of age effects for mothers and fathers, however, such a possibility appears unlikely to offer a complete explanation. In epidemiological studies of childhood disorders, age increases in prevalence rates are found for all disorders in childhood, including both internalizing and externalizing disorders (Anderson & Werry, 1994). Despite this pattern of generally increasing prevalence rates, however, positive age effects in our study were generally found for paternal psychopathology, whereas negative age effects were generally found for maternal psychopathology. A general impact of raising prevalence rates of childhood disorders would predict similar positive age effects for mothers and fathers.

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practical significance of these disorders for children. Thus, although results generally show that it is important to attend to disorders in both parents, prevalence rates suggest that depression and anxiety in women and ASPD and alcoholism in men may still warrant special attention because children are not equally likely to be exposed to these disorders in mothers and fathers. However, such differences in prevalence rates should not dictate an exclusive focus on disorders in mothers or fathers, as problems in both mothers and fathers appear to be related to the presence of problems in children. Furthermore, it is possible that differences in base rates of disorders in men and women may be related to effect sizes in other ways, as disorders that are relatively rare in one sex (e.g., ASPD in women) may be more difficult to examine with representative samples. Other than these two sets of findings bearing on theoretically important differences between maternal and paternal psychopathology, most of the significant differences across groups of effects were related to methodological differences across studies, including the method of assessing mental health problems in parents and children, the type of sample recruited, and familial composition. We discuss these methodological factors in turn. Several differences in the method of assessing mental health problems in parents and children across studies were found to be related to the magnitude of effects. At the broadest level, studies relying on symptom ratings for parent or child mental health problems tended to find larger effects than studies relying on a diagnostically based categorical approach to assessment of parents or children. However, the approach to assessment was frequently the same within studies for parents and children. Examination of the unique effects for each revealed that differences in the method of assessing parental psychopathology appeared to be most relevant for internalizing problems, whereas differences in the method of assessing childrens problems appeared to be most relevant for externalizing problems. Furthermore, substantial variability was found within all subgroups of these broad analyses, some of which was related to differences across studies in terms of the informant for symptomatic or diagnostic information. For the diagnostic assessment of parents, differences in the magnitude of effects across studies were related to differences in the informant. However, the small number of studies using assessment methods other than self-report (especially for mothers) limits the ability to arrive at substantive conclusions regarding differences across approaches to assessing mental health diagnoses in parents. Results tentatively suggest that research relying solely on spousal reports for diagnostic information on fathers may lead to diminished effects relative to studies using other assessment methods. At the very least, it appears that careful attention to the methods of diagnosing parents is warranted when interpreting the results of research on the association between psychopathology in parents and children. For studies that used symptom ratings to assess internalizing or externalizing problems in children, those that relied on parental reports tended to yield the largest effects. Such findings are consistent with several explanations, including the possibilities that the presence of parental psychopathology may lead to biased reporting by parents, that parents may be more sensitive than other informants to the presence of behavior problems in children, or that childrens behavior may vary across situations such that differences across raters may reflect actual differences in chil-

drens behavior across settings. It is worth noting that the magnitude of effects from teacher ratings appeared to differ for internalizing and externalizing disorders, such that teacher ratings of internalizing disorders yielded the smallest effects, whereas teacher ratings for externalizing disorders yielded effects that were among the largest. This pattern may reflect the possibility that teachers are less sensitive to internalizing problems in children, as such problems may be less overtly noticeable or disruptive to classroom functioning. Differences in the magnitude of effects across raters highlight the importance of including multiple informants of emotional and behavior symptoms, as the use of multiple informants allows researchers to avoid the potential source confound inherent in having parents rate both their own and their childrens psychological symptoms (Achenbach et al., 1987). The informant for childrens internalizing and externalizing disorders also was related to differences in the magnitude of effects across studies. For externalizing disorders, studies relying directly on childrens reports yielded the largest effects. For internalizing diagnoses, similarly, studies collecting diagnostic information directly from children yielded larger effects than studies relying on parent report or medical records, although such effects were not larger than those from studies combining information from multiple informants. It is noteworthy that the pattern of results for the source of diagnostic information on children differed somewhat from the pattern of results found for the source of symptom ratings for children in that studies collecting diagnostic information directly from children yielded results that were among the largest, whereas studies relying on childrens self-reports on symptom-based questionnaires yielded effects that were among the smallest. It may be that children are able to provide more complete and reliable information about their problems in the context of a sensitive, probing interview than they are able to provide in response to questionnaires. As for symptom-based studies, however, differences in the magnitude of effects across each informant for childrens diagnoses highlight the need to collect information from multiple informants to provide a more complete assessment of childrens functioning. Another methodological factor related to differences in the magnitude of effects across studies was the type of sample used by researchers. For externalizing problems (but not for internalizing problems), the difference between parent clinical and child clinical samples was significant when the effects of other moderators was controlled. In light of the substantial variability of sample type within subgroups of studies and in light of the fact that differences for internalizing problems were not significant when other moderators were controlled, substantive interpretations of differences across types of samples should be made cautiously. Nevertheless, differences found between samples of clinically referred parents and either samples of clinically referred children or community samples were partially consistent with predictions and point to the possibility that there may be systematic differences between samples of clinically referred parents and children referred for externalizing problems, which remain to be specifically addressed in the literature. In addition to the method of assessing parents and children and the sample type, the family composition in samples studied was also related to differences in the magnitude of the findings. Although we had predicted that the effects of family composition on the magnitude of effects would differ for mothers and fathers, this

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hypothesis was not supported. Rather, results for mothers and fathers generally indicate that samples composed mostly of singleparent families yielded effects that were not significantly different from those samples composed entirely of intact families, and both yielded effects that were larger than samples in the middle range of family composition, although analyses for fathers were limited by the small number of studies using predominantly single-parent families. It is possible that different processes account for the larger magnitude of findings from families at either end of the spectrum of family composition, although studies specifically addressing differences between familial transmission of psychopathology in different family arrangements are needed. For instance, there may be greater opportunities for family conflict in intact families (a common correlate of parental psychopathology), which may be related to higher levels of emotional problems in children. However, in single-parent families, either the greater time spent with the affected parent or the level of contextual stress of living in a single-parent family may play larger roles in explaining the magnitude of effects. Although this meta-analysis represents the first comprehensive attempt to compare the influences of psychological disorders in mothers and fathers on the development of emotional and behavior problems in their children, several limitations must be acknowledged. First, it is possible that results may have been attenuated by focusing exclusively on broadband syndromes of behavior problems in children rather than on specific childhood disorders, as it is possible that the pattern of association between parent and child psychopathology may vary across specific disorders. In general, however, there is only consistent evidence for such specificity within the externalizing disorders, as evidence exists supporting the distinct family histories of ADHD versus ODD/CD children. To examine the distinctiveness of specific externalizing disorders, research examining children screened for comorbid diagnoses is required. Because only four such studies were included in our sample of studies (Lahey et al., 1988; Nigg & Hinshaw, 1998; Reeves, Werry, Elkind, & Zametkin, 1987; Stewart, DeBlois, & Cummings, 1980), quantitative analyses of possible differences between children with pure ADHD diagnoses and other externalizing disorders were not possible. Qualitatively, the results of these studies are generally consistent with the notion that pure ADHD may be less strongly related to parental psychopathology than either comorbid ADHD or ODD/CD. In three of the four available studies (Lahey et al., 1988; Reeves et al., 1987; Stewart et al., 1980), the rates of paternal and maternal psychopathology were not found to be elevated for pure ADHD children but were significantly higher for children with CD or comorbid ADHD/CD.6 Thus, the inclusion of families with children with ADHD in the present meta-analysis may slightly attenuate the results. However, because comorbidity rates for ADHD tend to be high, the majority of studies did not screen for comorbidity in children, and only four studies with pure ADHD were included, this attenuation is not likely to greatly affect the present findings. Nevertheless, in light of the consistent findings for the different pattern of familial psychopathology in children with ADHD versus children with ODD/CD, it is important for future researchers to address such comorbidity in their samples of children. Second, specific mental disorders in parents and children were treated independently. In reality, comorbidity of disorders is common both in children and adults. For instance, children with

internalizing disorders are commonly found to be comorbid for externalizing disorders and vice versa (e.g., Wright, Zakarski, & Drinkwater, 1999). Although parental psychopathology was, in general, similarly associated with both internalizing and externalizing disorders, such results may either reflect that the risk factors operate similarly for the two types of child behavior problems or that such problems tend to co-occur in children. Similarly, differences across specific parental disorders in relation to the presence of internalizing or externalizing disorders should be interpreted cautiously, as few studies controlled for comorbid parental diagnoses. Third, disorders in mothers and fathers were treated independently in the meta-analysis, though in reality mental health problems tend to co-occur in mothers and fathers, a phenomenon referred to as assortative mating (Merikangas & Brunetto, 1996). The majority of studies included mothers and fathers from the same family without controlling for spousal diagnoses. As such, the effect sizes from one parent are likely to include some risk from an affected partner, potentially increasing the childrens genetic risk for disorder and exposing children to more dysfunctional parenting and stressful environments. Conversely, the presence of a healthy partner may moderate some of the risk to children, either through lower genetic risk than in dually affected families, through healthy parenting by at least one parent, or through buffering parenting practices that may protect the child from the negative consequences of disturbance in the other parent. Consistent with such possibilities, several studies have found higher rates of internalizing and externalizing disorders in children whose parents both exhibit mental health problems (including depression and substance use disorders) relative to children with only one affected parent (Dierker et al., 1999; Goodman, Brogan, Lynch, & Fielding, 1993; Reich, Earls, Frankel, & Shayka, 1993). Most notable is a recent large-scale study in which Foley and colleagues (2001) used a genetically sensitive design to find different patterns of association between maternal and paternal disorders, including depression and alcoholism, with internalizing and externalizing disorders depending on the presence or absence of disorders in spouses and higher rates of disorder and a wider range of disorders present in the offspring of dually affected parents. Together, these findings highlight the need for researchers to include the mental health of the spouse as an important moderator variable in future studies and indicate that the present review may be limited by the failure of the majority of studies to do so. Though several limitations exist, this meta-analysis marks an important step in examining a domain of family influence that has been too often overlookednamely, that of fathers and, specifically, fathers psychological problems. This review marks the first comprehensive quantitative comparison of the influence of psychopathology in mothers and fathers in the development of emotional and behavior problems in children. Contrary to the motherblaming traditions of psychology, we offered persuasive evidence that the risk for psychopathology in children associated with
6

Nigg and Hinshaws (1998) results differed somewhat from this general pattern, as ADHD was found to be related to the presence of maternal depression and anxiety regardless of childrens comorbidity status. However, as no other maternal or paternal diagnoses were found to be related to pure ADHD, some consistency across even this study is seen.

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psychological disturbance in fathers is generally as strong as when the disturbed parent is the mother, although some differences across parental disorders were noted. Indeed, the variability of effects appears to be more closely related to methodological differences across studies than to differences across the gender of the affected parent. The results of the present meta-analysis lead to several suggestions for future research. First, researchers should make more of an effort to include both mothers and fathers in their samples. It is no longer justifiable to exclude fathers from research programs on the basis of the belief that their mental health problems are less closely related to childrens problems than are mothers. Furthermore, in light of the differences in the effects of child age on the magnitude of effects for mothers and fathers and of the magnitude of effect sizes for depression and alcohol and substance abuse disorders based on the gender of the affected parent, it is necessary for researchers to specify the gender of the affected parent in their analyses rather than report findings for a mixed group of mothers and fathers. The interaction of mental health problems in mothers and fathers should also be more heavily studied to examine the mechanisms through which a healthy parent may buffer children from psychopathology in the other parent. Second, studies of the association between parental psychopathology and childrens emotional and behavior problems should make more of an effort to examine boys and girls separately. Though few differences between effect sizes for boys and girls were found in the present review, the vast majority of studies either focused exclusively on behavior problems in boys or grouped boys and girls together in their analyses, limiting the ability of the present review to examine gender differences with sufficient power. Third, the field would benefit from increased emphasis on possible moderators of the relationship between psychopathology in mothers and fathers and the presence of emotional and behavior problems in children, particularly in light of the generally small magnitude of effect sizes for both mothers and fathers. The small magnitude of effects for both mothers and fathers highlights the need for researchers to examine variables that may either protect children from the effects of psychopathology in mothers or fathers or place them at heightened risk. Potential moderators of interest include not only the mental health of the spouse, as discussed above, but also individual characteristics of the child. For example, child temperament may interact with parental psychopathology in leading to the development of child behavior problems and may prove to be important in explaining the generally small magnitude of the present results. Belsky, Hsieh, and Crnic (1998) argued that children with difficult or inhibited temperaments may be more susceptible to variations in parenting quality than are other children. As such, children with difficult early temperaments may be more strongly influenced by the presence of psychopathology in parents than are children with easier temperaments, and the generally small magnitude of the effect sizes may in part be the result of studies collapsing across children who are more and less affected by parental psychopathology. Belsky et al. found support for the interaction of parenting quality and child temperament for the development of internalizing and externalizing problems in children. However, little evidence exists that is specific to parental psychopathology per se. In one of the few attempts to examine such an interaction, Blackson, Tarter, and Mezzich (1996) studied

parental discipline practices and child temperament in predicting internalizing and externalizing behavior problems in 10 12-yearold boys of substance-abusing fathers and found that difficult child temperament placed children at risk for harsh discipline by substance-abusing fathers and was associated with elevated rates of internalizing and externalizing problems. Finally, researchers should place greater emphasis on examining the pathways between mental health problems in mothers and fathers and the development of emotional and behavior problems in boys and girls. In particular, research should examine the mechanisms of the difference between mental health problems in mothers and fathers in an effort to understand differences in the magnitude of effects of maternal versus paternal psychopathology on the basis of childrens age and why some forms of psychopathology appear to represent larger sources of risk for children when they are present in mothers versus fathers. As demonstrated in the present meta-analysis, Goodman and Gotlibs (1999) model may provide a good starting point for such research. In following these suggestions, future research should help researchers understand the nature of the risk for the development of emotional and behavior problems in children with emotionally disturbed parents and may ultimately lead to improved prevention and intervention efforts.

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Appendix Characteristics of Studies in Meta-Analytic Sample

Study Allen et al. (1998) Ammerman et al. (1994) Blackson et al. (1994, 1996) Moss et al. (1992, 1994, 1995, 1997) Tarter, Blackson, Martin, Loeber, & Mossirt (1993) Tarter, Blackson, Martin, Seilhamer, et al. (1993) C. Anderson & Hammen (1993) Banez & Compas (1990) Barrera et al. (1993) Bell & Cohen (1981) Beng et al. (1974) Bird et al. (1989) Briggs-Gowan et al. (1996) Brock et al. (1996) Carbonneau et al. (1998) Carro et al. (1993) Carter et al. (2001) Christ et al. (1990) Cicchetti et al. (1998) Clark et al. (1997) Cody & Fitzgerald (1989) Cole & Rehm (1986) Compas et al. (1991) Cooper & Eke (1999) Cunningham et al. (1988) Davies & Windle (1997) Dawson (1992) Dierker et al. (1999) Ellis (1992) Fergusson et al. (1993) Forehand et al. (1986) Forehand & Smith (1986) Frick et al. (1989) Frick et al. (1992) Frick et al. (1994) Friedman (1974) Gittelman-Klein (1975) Goodman (1987) Gray (1988) Hamdan-Allen, Stewart, & Beeghly (1989) Hammen & Brennan (2001) Hammen et al. (1987) Harden & Pihl (1995) Harnish et al. (1995) Hibbs et al. (1992) Hill & Muka (1996) Iacano et al. (1999) Shiner & Marmostein (1998) N 579 175 Child age 16.40 10.95 Sample Community Clinical Parent Mother Father Parent rating Sx Dx Parental disorder Mix Alc Child gender Mix Boy Child rating Dx Dx Child problem Int and Ext Int and Ext

78 69 296 49 213 386 188 115 642 70 69 253 156 283 33 45 309 128 52 443 3,409 126 128 128 768 46 36 66 177 95 95 33 84 153 636 191 110 58 28 386 101 76 520

12.00 9.74 12.70 9.83 9.00 10.00 10.30 2.00 6.12 2.67 2.50 14.50 1.70 11.00 14.50 10.00 12.00 4.00 9.92 15.50 11.00 12.30 4.10 4.10 12.50 13.50 12.83 14.50 9.50 7.00 11.00 4.00 9.20 2.50 10.00 11.35 15.17 12.66 12.10 6.52 13.25 11.30 17.00

Clinical Community Community Clinical Clinical Community Community Community Community Community Community Clinical Community Clinical Clinical Clinical Community Community Clinical Community Community Clinical Community Community Community Community Community Clinical Clinical Clinical Clinical Clinical Clinical Clinical Community Clinical Community Clinical Clinical Community Clinical Clinical Community

Mother Both Father Mother Mother Both Mother Both Father Both Mother Both Mother Father Mother Both Both Mother Both Mother Both Both Father Father Mother Both Both Mother Both Mother Mother Mother Both Mother Mother Both Mother Mother Father Mother Both Mother Both

Dx Sx Dx Dx Dx Dx Sx Dx Dx Sx Dx Sx Dx Dx Dx Dx Sx Dx Sx Sx Dx Dx Dx Dx Sx Sx Sx Sx Dx Dx Dx Sx Dx Sx Sx Dx Sx Dx Dx Sx Dx Dx Dx

Dep, Bip Mix Alc Alc Dep, Mix Mix Dep, Anx Alc Alc Dep Dep ASPD Dep Alc Dep Alc, Dep, Anx, ASPD Dep, Anx, Scz Dep, Anx Dep Dep Alc Alc, Mix Alc Alc Dep Dep Dep ASPD Alc, Dep, ASPD Anx Anx Dep, ASPD, Scz, Bip Dep, Anx Dep, Scz Alc, Dep, Anx Alc, ASPD Dep Dep, Bip Alc Dep Mix Alc Alc, Dep

Mix Mix Mix Mix Both Mix Both Mix Boy Mix Both Boy Mix Boy Mix Mix Mix Mix Mix Both Mix Mix Boy Boy Mix Mix Girl Boy Mix Mix Mix Mix Mix Mix Mix Boy Mix Mix Boy Mix Mix Mix Both

Sx Sx Sx Sx Dx Dx Sx Sx Sx Sx Sx Sx Sx Dx Sx Dx Sx Sx Dx Sx Sx Dx Sx Sx Sx Sx Sx Sx Dx Dx Dx Sx Dx Dx Sx Dx Dx Dx Sx Sx Dx Dx Dx

Int and Ext Int Ext Ext Int Int and Ext Int and Ext Int Int and Int and Int and Ext Int and Int and Ext Ext Ext Ext Ext Ext

Int Int and Ext Int Ext Int and Ext Ext Int and Ext Int Ext Ext Int and Ext Int Ext Ext Int Int Int and Ext Int Int and Ext Int Ext Int Int and Int and Ext Ext Int and Int and Ext Ext Ext Ext

(Appendix continues)

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Appendix (continued)
Study Jackson (1994) Jackson (1999) Jackson et al. (1998) Jacob & Johnson (1997) Jacob & Leonard (1986) Jensen et al. (1990) Jensen et al. (1988) Johnson & Jacob (1995) Johnston (1991) Kamstra (1986) Kaslow et al. (1988) Keller et al. (1986) Klein & Forehand (2000) Kochanska (1990) Kostyak (1987) Kovacs et al. (1989) Krain & Kendall (2000) Lahey et al. (1988) Last, Hersen, et al. (1987) Last, Phillips, & Statfeld (1987) Last & Strauss (1989) Lavori et al. (1988) Little et al. (2001) Lang et al. (1996) Lothstein (1990) Luthar et al. (1998) Manassis & Hood (1998) Marchand & Hock (1998) Martin & Burchinal (1992) Messer & Beidel (1994) Mick et al. (2000) Mitchell et al. (1989) Najman et al. (2000) Nash & Johnston (1983) Nigg & Hinshaw (1998) OConnor & Kaskari (2000) Offord et al. (1979) Poleshuck (1998) Puttler et al. (1998) Radke-Yarrow et al. (1992) Reeves et al. (1987) Renk et al. (1999) Sawyer et al. (1998) Schachar & Wachsmuth (1990) Schaughency & Lahey (1985) Shaw et al. (1994) Singer et al. (1998) Spieker et al. (1999) Steinhausen et al. (1984) Stern (1982) Stewart et al. (1980) Stewart & Leone (1978) Stormont-Spungin & Zentall (1995) Suqwara (1997) N 111 188 100 56 268 59 178 34 33 40 37 212 56 90 104 138 86 73 97 17 143 91 29 54 119 74 46 1,425 65 273 117 7,421 91 132 41 146 107 106 100 190 150 696 63 61 100 123 176 58 27 118 36 63 114 Child age 3.50 4.70 13.74 14.00 8.92 8.90 12.30 8.50 9.39 9.70 16.00 8.92 5.00 11.50 11.2 11.09 9.31 9.10 9.40 16.10 14.00 12.20 3.70 4.50 11.7 9.80 4.00 7.45 9.75 11.50 12.00 14.00 6.94 9.20 5.50 13.82 4.81 4.00 2.50 8.84 13.65 12.50 9.00 9.50 3.00 2.00 3.50 9.00 6.60 9.48 9.10 4.00 8.52 Sample Community Community Community Community Clinical Community Community Clinical Clinical Clinical Clinical Community Community Community Community Clinical Clinical Clinical Clinical Clinical Clinical Community Clinical Clinical Clinical Clinical Community Community Community Clinical Clinical Community Clinical Clinical Clinical Clinical Community Community Community Clinical Community Community Clinical Clinical Community Community Community Clinical Clinical Clinical Clinical Community Community Parent Mother Mother Both Father Both Both Mother Mother Father Both Both Mother Mother Both Mother Both Mother Mother Mother Mother Both Mother Mother Mother Mother Mother Both Mother Both Mother Both Mother Mother Both Mother Both Both Father Mother Both Both Both Both Both Mother Mother Mother Both Mother Both Both Mother Mother Parent rating Sx Sx Dx Dx Sx Sx Sx Sx Dx Sx Dx Sx Dx Dx Sx Sx Dx Dx Sx Dx Dx Sx Sx Sx Dx Sx Sx Sx Sx Dx Dx Dx Sx Dx Sx Dx Sx Dx Dx Dx Dx Sx Dx Sx Sx Sx Sx Dx Dx Dx Dx Sx Dx Parental disorder Dep Dep Dep Alc, Dep Mix Mix Dep, Alc Dep Alc Dep Dep Dep Dep Alc Dep, Anx, Mix Anx Dep, Bip, Anx, Alc, ASPD Alc, Dep, Anx Anx Anx Dep Dep Dep Dep Mix Anx Dep ASPD Dep, Anx, Mix Dep Alc, Dep, Anx, ASPD, Scz Dep, Anx Dep Dep, Anx, ASPD, Bip Alc, Dep Mix Dep Alc Dep, Bip Anx, Alc, ASPD Dep Mix Mix Dep Dep Dep Mix Alc Dep Dep, Anx, Alc Alc, ASPD, Mix Dep Dep Child gender Mix Mix Mix Both Mix Both Both Mix Both Mix Mix Mix Mix Mix Mix Both Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Mix Boy Mix Boy Mix Both Mix Mix Both Mix Boy Mix Both Mix Mix Mix Mix Boy Boy Boy Mix Child rating Sx Sx Sx Sx Sx Sx Sx Sx Sx Dx Dx Sx Sx Sx Dx Sx Dx Dx Dx Dx Dx Sx Sx Sx Sx Sx Sx Sx Dx Dx Dx Sx Sx Dx Sx Dx Sx Sx Dx Dx Sx Sx Dx Sx Sx Sx Sx Sx Sx Dx Dx Sx Dx Child problem Ext Ext Int and Int and Int Int and Int and Int and Int Int Int Int and Ext Int and Int Int and Ext Int Int Int Int Int Int Int Int Int Int Ext Ext Ext Ext Ext

Ext Ext Ext

and and and and and and

Ext Ext Ext Ext Ext Ext

Int and Ext Int Ext Int Int and Ext Int and Ext Ext Int Ext Int and Ext Int and Ext Int and Ext Int and Ext Int and Ext Int and Ext Ext Int and Ext Int and Int and Ext Int and Int and Ext Ext Ext Int Ext Ext Ext Ext

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Appendix (continued)
Study Tambs & Moum (1993) Tanenbaum & Forehand (1994) Thomas & Forehand (1991, 1993) Tisher et al. (1994) Tubman (1991, 1993) Udayakum et al. (1984) Vanyukov et al. (1993) Vitaro et al. (1996) Warren et al. (1997) Webster-Stratton (1988) Webster-Stratton (1996) Weissman et al. (1999) Weller et al. (1994) Welner & Rice (1988) Whaley (1998) Windheuser (1977) Windle & Dumenci (1998) Wright (1985) Zima et al. (1996) N 9,384 282 115 154 53 100 150 437 172 120 220 108 59 76 36 94 257 207 157 Child age 10.00 12.75 13.10 9.00 7.75 10.50 10.90 6.00 17.50 4.33 4.81 13.2 9.00 11.72 10.25 14.50 15.50 17.50 9.00 Sample Clinical Community Community Clinical Community Clinical Clinical Community Community Clinical Clinical Clinical Clinical Clinical Clinical Clinical Community Community Community Parent Both Mother Both Both Both Father Both Father Mother Both Both Mother Both Both Mother Mother Mother Both Mother Parent rating Sx Sx Sx Sx Sx Dx Sx Dx Sx Sx Sx Dx Dx Dx Sx Dx Sx Sx Dx Parental disorder Dep Dep Dep Dep Dep, Alc Alc ASPD, Alc Alc Anx Dep Alc, Dep Mix Alc, Dep, Anx, Scz, ASPD Alc, Dep Dep, Anx Anx Dep Alc Alc, Dep Child gender Both Mix Both Mix Both Mix Boy Mix Mix Mix Both Mix Mix Mix Mix Mix Both Mix Mix Child rating Sx Sx Sx Dx Sx Sx Dx Sx Dx Sx Dx Dx Dx Dx Sx Sx Sx Sx Sx Child problem Int Int and Ext Int and Ext Int Int and Int and Ext Int and Int Int and Ext Int and Int Ext Ext Ext Ext Ext

Int and Ext Int Int Int Int Int and Ext

Note. Sx symptom based; Dx diagnosis based; Int internalizing; Ext externalizing; Alc alcohol or substance abuse; Dep depression; Bip bipolar disorder; Anx anxiety; ASPD antisocial personality disorder; Scz schicophrenia.

Received May 22, 2000 Revision received February 27, 2002 Accepted February 28, 2002