Fathers' behaviours and children's problems
The last two decades have witnessed a growing concern and interest in the role that fathers play in the lives of their children. How does family life – particularly aspects such as biological fathers’ non-residence, and fathers’ parenting – impact upon children’s psychopathology? The three broad theoretical perspectives that drive research in this area are the standard family environment model, the passive genetic model, and the child effects model. This article discusses the empirical evidence and concludes that to move the field forward future studies need to appropriately compare these three competing theoretical perspectives.
Families have changed considerably since the 1970s, and the effects of these changes, especially on children, have been the subject of heated debate. Such debate is mostly about the consequences of parental separation or divorce for children, and the evidence debated is provided by studies adopting one of three competing theoretical perspectives.
The most popular perspective, the standard family environment model, assumes that many single-parent families formed through parental separation are less than optimal settings for children’s socialisation and development and that exposure to these environments increases the risk of a variety of problems.
The second perspective, the passive genetic model, assumes that parents’ and children’s behaviours are linked becauseof the transmission of genes from parents to children. Parents with problematic personality traits, such as neuroticism or a predisposition to engage in antisocial behaviour, are more likely than other parents to experience inter-parental conflict and separation. Because parents transmit these traits to their biological children genetically, children in these families are prone to a variety of difficulties. Therefore, the links are spurious as the causal mechanism connecting these parental and child behaviours is genetically inherited predispositions.
Finally, the child effects model (Amato & Cheadle, 2008) also challenges the standard family environment model by pointing out that, as the vast majority of studies in this literature involves correlations derived from cross-sectional data, the alternative explanation that children’s behaviour is the cause rather than the result of parental separation is plausible.
With the increasing availability of genetically sensitive longitudinal studies, it is now possible to compare the theoretical models for linking children’s psychopathology and aspects of parenting such as fathers’ non-residence and fathers’ parenting. However, as will be discussed below, very few studies compare all three models. The lack of research comparing these alternative theoretical perspectives is unfortunate, as the findings of such comparisons will have important implications for both theory development and intervention design.
The absent father
Moynihan’s (1965) ‘pathology of the matriarchy’ hypothesis stated that the absence of a father is destructive to children, particularly boys, because it means that they will lack the economic resources, role models, discipline, structure and guidance that a father provides. A great deal of evidence has been collected since the 1970s to either support or refute this, so we now know a lot about links between children’s internalising and externalising behaviour problems in single-mother families, and we are increasingly building knowledge about the adjustment of children in single-father families. For example, explorations of the association between family structure and alcohol use (Bjarnason et al., 2003a) and smoking (Bjarnason et al., 2003b) in adolescents from 11 European countries showed that, although adolescents living with both biological parents engaged less frequently in heavy alcohol use and smoked less than those living in any other arrangements, adolescents living with a single mother both drank and smoked less than those living with a single father or with neither biological parent. Recent American research reveals a similar picture: although adolescents in single-parent families are more delinquent than their counterparts residing with two biological parents, adolescents from single-father families are significantly more delinquent than those living in single-mother families (Demuth & Brown, 2004), and although adolescents in single-parent or step-parent families are at heightened risk of drug use, adolescents living in single-father families are at risk of both higher levels of use and increasing use over time (Hoffmann, 2002).
In fact, although the general conclusion from studies carried out since the 1970s is that children experiencing family disruption carry a heightened risk of short- and long-term adverse psychological outcomes, this risk is not consistent and it is modified by various factors. For example, it is modified by the number and timing of parents’ partnership transitions. In a longitudinal study of children from kindergarten to 10th grade, Lansford et al. (2006) showed that parental divorce during elementary school was more negatively related to trajectories of children’s internalising and externalising behaviour problems than was later divorce/ separation, which was in turn more negatively related to children’s school grades. Effects are also modified by the pathway into single parenthood (e.g. via parental separation or via parental death) and by the structure of the family following disruption (Hofferth, 2006), with children’s psychological adjustment being, on average, worse in stepfamilies than in single-mother families. The general consensus is that the deterioration of economic conditions that usually results from family disruption is the major explanation for children’s lower ability and achievement, although not necessarily for children’s internalising and externalising behaviour problems, following parental divorce or separation. However, the finding that the effect of parental death on children is typically smaller (less negative) than the effect of parental divorce (Biblarz & Gottainer, 2000) is also consistent with the argument that at least some of the divorce effect is due to selection.
According to the selection perspective, inherent characteristics of parents, such as antisocial personality traits, are direct causes of dysfunctional family patterns and divorce, as well as child problems. To the extent that parents’ personalities and genetically transmitted predispositions are causes of divorce as well as child problems, the apparent effects of divorce on children are spurious.
By using genetically sensitive study designs, recent research has started to address this issue of selection effects systematically and to shed new light in the divorce–child adjustment link. For example, D’Onofrio and colleagues (2006) showed that, in their sample of children of twins discordant for divorce (the offspring of divorced parents are compared with their cousins whose parents remained married), divorce was related to educational problems, depressed mood, suicidal ideation, and earlier initiation of sexual intercourse and emotional problems. However, the increased risk of earlier initiation of drug use among children who had experienced parental divorce was explained by selection factors, including genetic confounds. The general conclusion so far from several studies comparing appropriately the standard family environment model with the passive genetic model is that the origin of the association between divorce and child psychopathology is shared environmental in origin (Burt, 2009, for a review).
However, as mentioned earlier, very little research activity has been devoted to comparing all three alternative models. One exception is Amato and Cheadle’s (2008) study, which, using data from adopted and biological children from the first two waves of the National Survey of Families and Households, also found strong support for the standard family environment model.
There is less research on fathers’ parenting and child psychopathology, and it usually follows the assumptions of the tandard family environment model.
Of great importance in this literature is the evidence from studies testing moderator (interaction) effects on paternal’ parenting/child psychopathology associations. For example, researchers started testing such associations by family structure almost as soon they became interested in the role of fathers in child development, and studies now routinely model the effect of the interaction between fathering and mothering on child psychopathology. Research on resilience has also established the importance of distinguishing between fathers’ and mothers’ parenting when modelling the moderator effect of parenting on children’s positive adaptation in the face of specific (e.g. Brennan et al., 2003: maternal depression) and cumulative
(e.g. Ge et al., 2009: number of adverse life events) contextual risk.
The standard family environment model
Research following the assumptions of the standard family environment model has both increased and improved in several ways over the last decade.
Firstly, more studies have emphasised specificity. For example, we now know that although levels of paternal support are related to levels of internalising behaviour problems in children (Bean et al., 2006), in limiting externalising behaviour problems it’s paternal behavioural control rather than support that is most effective (Galambos et al., 2003).
Secondly, studies are increasingly examining the role not only of absolute but also of differential parenting in children’s outcomes. Although, with few exceptions (e.g. Atzaba-Poria & Pike, 2008), most of this research considers only maternal parenting, some of the recent findings of studies looking at fathers’ differential parenting and at within-family differences in fathers’ and mothers’ parenting are impressive. Tamrouti-Makkink et al. (2004), for instance, found no direct association between differential parental treatment and child outcomes above the absolute levels of parenting in same-gender sibling pairs. But when looking at mixed-gender sibling pairs, differential maternal and paternal control was related to internalising behaviour of girls and differential paternal warmth to externalising behaviour of the older siblings.
Thirdly, more studies have tested moderator effects. Not only has this improved understanding of how fathers’ parenting and children’s behaviours are related, but it has also helped identify specific groups for intervention. Influential reviews by Lamb (2000) and Parke (2000) concluded that a focus on paternal nurturance, with little attention paid to other functions or aspects of fatherhood, ignores subcultural variation in the definition and understanding of fatherhood. As a result, studies now increasingly consider demographic and cultural or subcultural specificity when modelling fathering–child adjustment links. For example, ethnicity, which has been routinely explored as a moderator in studies linking fathers’ parenting and children’s behaviour in the US, has started to receive attention in the UK (Deater-Deckard et al., 2004) as well.
However, there is very limited research testing moderator effects on child behaviour links with certain important fathering dimensions, such as economic providing. Although there has been a lot of research linking fathers’ absence of economic providing with children’s psychological outcomes, particularly externalising behaviour problems (Amato & Gilbreth, 1999) in father-absent families, we know very little about the role of fathers’ economic providing in father-present families and even less on the moderator effect of fathers’ characteristics on the association between fathers’ income and children’s outcomes. This is important, as a fathers’ income may not be associated with positive child outcomes when the father, for instance, does not contribute to household expenses or his consumption of resources drains the family budget especially if he spends the family’s funds on personal items or services (Engle & Breaux, 1998).
The child effects and the passive genetic models
In contrast to the significant increase in the number of recent studies testing father-to-child effects, only few studies have tested child-to-father effects (e.g. Hawkins et al., 2007; Jaffee et al., 2004), and even fewer have compared the child effects model with the other two theoretical models. In a study of adolescent adoptees and their families, Ge et al. (1996), for instance, measured adoptees’ genetic risk for antisocial behaviour on the basis of their biological parents’ psychopathology. They found that these adopted children elicited more harsh and inconsistent discipline and less nurturant and involved parenting from their adoptive parents compared with adopted children whose biological parents did not have a history of disorder. Although the data were cross-sectional, the researchers also suggested reciprocal parent–child effects: adoptees’ antisocial behaviour was influenced by and was an influence on mothers’ (but not fathers’) negative parenting. More recently, Hawkins et al. (2007) used nationally representative data from the 1995 and 1996 waves of the National Longitudinal Study of Adolescent Health to estimate the associations between non-resident fathers’ involvement and adolescents’ psychopathology and achievement. They argued that their results supported a child effects rather than a father effects model. In the UK, Lifford et al. (2008) used cross-lagged panel correlation and reciprocal effects analysis in a longitudinal sample of school children and their parents to show differences in the direction of effects linking mother– and father–child rejection and child ADHD symptoms, with ADHD symptoms affecting the mother–child relationship and the converse pattern of effects noted for fathers.
Still, what is needed to address the issue of comparing all three competing theoretical perspectives discussed above is longitudinal studies of fathers’ parenting and children’s adjustment in samples that include good measures of genetic risk and children from both biological and adoptive families. I am not aware of any such study.
Child psychopathology and fathers’ psychopathology
The role of paternal psychopathology in child psychopathology has been examined in studies since the 1980s, although a lot of progress was made after Phares and Compas (1992) voiced the need to routinely explore paternal psychopathology when studying child psychopathology. A decade later Connell and Goodman’s (2002) meta-analysis concluded that, although children’s internalising problems appear to be linked more closely to maternal than
to paternal psychopathology, children’s externalising behaviour problems appear to be linked in comparable ways to mothers’ and fathers’ psychopathology. Many of the studies modelling the association between parental and child psychopathology include paternal parenting as an intervening variable, testing the effect of paternal depression or substance abuse on paternal parenting (Ramchandani & Psychogiou, 2009, for a review). Some recent studies have explored links with other, less well researched in this literature, paternal psychiatric disorders, such as ADHD (Harvey et al., 2003).
The progress in research on child and paternal psychopathology over the last decade or so has been phenomenal. Studies, for instance, now test links between paternal childhood psychiatric disorders and offspring psychopathology in view of the evidence that parental childhood psychiatric disorders may be more strongly predictive of children’s index case psychiatric disorders than are parental adulthood psychiatric or substance use disorders (Clark et al., 1997). They also start to consider full specificity models of the association between paternal and child psychopathology. Still, the emphasis continues to be on the effect of fathers’ antisocial behaviour and substance abuse on child psychopathology (Kelley & Fals-Stewart, 2004), although fathers’ depressed mood (Cummings et al., 2005) has started to receive attention, too.
However, research using genetically sensitive study designs has generally not tested mutual influence models of paternal and child psychopathology, although general population studies testing such reciprocal effects have shown promising results. For example, Ge et al. (1995) showed that mutual influences on distress were significant and gender-specific, with the strongest cross-lagged associations occurring between mothers and sons and between fathers and daughters.
I have discussed some of the evidence for the links between child psychopathology and fathers’ residence/non-residence, parenting and psychopathology, and identified priorities for future research that will likely move forward not only the field of developmental psychopathology but that of child development as well. This section will now outline two issues that new research can easily address.
First, the range of child outcomes considered in child psychology and psychiatry studies exploring the role of fathers’ psychopathology, parenting, or residential transitions is still narrow. For example, we know little about fathers’ parenting and children’s treatment response or behavioural change (Beauchaine et al., 2005). Second, as discussed above, studies now routinely test the association between specific paternal parenting dimensions and specific child psychopathology, and the association between specific paternal psychopathology and specific child psychopathology. Recent studies have also emphasised the importance of testing links between specific paternal psychopathology and specific paternal parenting. However, studies rarely test full specificity in mediated models exploring the association between all three factors: paternal psychopathology, paternal parenting, and child psychopathology. This is a significant limitation, because understanding the mechanisms by which risk is transmitted in families is essential if successful interventions are to be developed. Addressing these issues and testing competing models of associations between fathers’ and children’s behaviours in future research can be challenging, but will be very exciting.
is at the Department of Psychology and Human Development, Institute of Education, University of London
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