Effect of parental MH on child MH

Although the aetiology of child psychopathology is multifactorial, the available literature indicates that exposure to parental psychopathology is a key determinant of mental disorders in children (McLaughlin et al., Reference McLaughlin, Gadermann, Hwang, Sampson, Al-Hamzawi, Andrade, Angermeyer, Benjet, Bromet, Bruffaerts, Caldas-de-Almeida, de Girolamo, de Graaf, Florescu, Gureje, Haro, Hinkov, Horiguchi, Hu, Karam and Kessler2012; Rasic et al., Reference Rasic, Hajek, Alda and Uher2014; Bellina et al., Reference Bellina, Grazioli, Garzitto, Mauri, Rosi, Molteni, Brambilla and Nobile2020). In the current study, there was a very strong relationship between the MH of parents and co-resident children, with children almost three-times more likely to report poor MH when one parent had poor MH, increasing to a 5-fold increase when both parents reported poor MH. This compares favourably with the existing body of literature; in a recent meta-analysis, Rasic et al., observed more than a two-fold increase in the risk of mental disorders in offspring of parents with severe mental illness, with even larger estimates observed for offspring with schizophrenia and bipolar disorder (Rasic et al., Reference Rasic, Hajek, Alda and Uher2014). Direct comparison of the current study is however challenging given the methodological heterogeneity across studies, including disparities in the measures used to identify mental illness, the age of offspring examined and the MH condition examined. Many of the previous studies also lacked statistical power or information on the MH status of the second parent.

In the last decade, our understanding of potential mechanisms for the familial transmission of mental illness has advanced with the emergence of genetically informed studies. Systematic reviews provide substantial evidence of the genetic transmission of MH disorders, including schizophrenia and depression (McAdams et al., Reference McAdams, Neiderhiser, Rijsdijk F, Narusyte, Lichtenstein and Eley2014; Jami et al., Reference Jami, Hammerschlag, Bartels and Middeldorp2021), though it is also clear that psychopathology may be transmitted through the shared rearing environment and through unique parent-child interactions. Parenting practices and family functioning have been highlighted as the primary drivers of environmental transmission of psychopathology and these factors are strongly correlated with offspring psychological wellbeing, with healthy offspring development heavily dependent on parental health and wellbeing (Berg-Nielsen et al., Reference Berg-Nielsen, Vikan and Dahl2002; Bradley and Vandell, Reference Bradley and Vandell2007; Bellina et al., Reference Bellina, Grazioli, Garzitto, Mauri, Rosi, Molteni, Brambilla and Nobile2020). In this administrative data-based study we were unable to contribute any insight into whether the increased risk for poor MH is a direct result of a shared genetic susceptibility, or an indirect effect of the impact of parental poor MH on the child's upbringing, from exposure to common stressors, witnessing mental ill-health episodes or the subsequent parenting style or parental involvement.

Effect of parental MH on child suicide

Personal poor MH remained the strongest independent risk factor for death by suicide in offspring even after adjustment for parental MH, contributing to more than a three-fold increase in the odds of suicide compared to those who did not report poor MH. This observation is consistent with findings from Danish studies where an up to 39-fold increase in the risk of suicide in offspring with a personal psychiatric hospitalisation was observed (Stenager and Qin, Reference Stenager and Qin2008; Sørensen et al., Reference Sørensen, Mortensen, Wang, Juel, Silverton and Mednick2009). Although a smaller magnitude of the effect was observed in this study, it is highly plausible that the identification of poor MH from a community-based self-reported measure would capture individuals with a wider range of mental ill-health conditions, including those considered less severe when compared to those requiring psychiatric inpatient admission, as is the case in the majority of studies examining this association. It is universally recognised by the authors of these studies that most cases with mild to moderate mental disorders are diagnosed and treated by general practitioners and will not be observed in such centralised psychiatric registers (Mors et al., Reference Mors, Perto, Preben and Mortensen2011).

The aetiology of the increased risk of mental illness and increased suicide risk in offspring of parents with mental illness are closely interlinked. Support for the implication of genetic transmission of risk for suicidal behaviours has been provided using a variety of study methodologies, including family studies, twin studies and adoptive studies (Mirkovic et al., Reference Mirkovic, Laurent, Podlipski, Frebourg, Cohen and Gerardin2016). Examination of the available evidence indicates significant heritability of suicide, estimated at an aggregated 45%, but this is highly dependent on the presence of psychiatric illness (Mirkovic et al., Reference Mirkovic, Laurent, Podlipski, Frebourg, Cohen and Gerardin2016). In addition, a wide range of environmental factors has been indicated in the development of suicidal behaviours, with the majority of studies attributing the increased risk to a wide range of early adverse experiences including maltreatment, interpersonal loss (e.g. parental death, separation) socio-economic adversity and family dysfunction (e.g. parental mental illness, domestic violence, incarceration) (Sahle et al., Reference Sahle, Reavley, Li, Morgan, Yap, Reupert and Jorm2021). Alterations in family functioning and parenting capacity owing to psychiatric illness may in turn increase exposure to these adverse childhood experiences, conferring a greater risk of internalising and externalising behaviours in exposed offspring(Hughes et al., Reference Hughes, Bellis, Hardcastle, Sethi, Butchart, Mikton, Jones and Dunne2017; Petruccelli et al., Reference Petruccelli, Davis and Berman2019), which are important risk factors for SRTs and behaviours among young people (Goodday et al., Reference Goodday, Shuldiner, Bondy and Rhodes2019).

We observed an elevated risk of suicide where both parents reported poor MH, which corroborates with Webb et al., who noted a 6-fold increase in offspring suicide where two parents had a recorded psychiatric inpatient record, compared to a 2–3-fold increase in those with one affected parent (Webb et al., Reference Webb, Pickles, Appleby, Mortensen and Abel2007). While this may represent increased genetic potential it is also plausible that exposure to two parents with poor MH would also result in greater impairment of parenting capacity and a more dysfunctional family home environment. In order to disentangle this relationship, studies which account for possible genetic influences, such as adoption and children-of-twins designs are necessary. However, suicide is both a rare and sensitive outcome, thus achieving sufficient power to provide robust risk estimates is challenging, even in large population-wide studies.

Whilst the association between parental and offspring MH persisted for both younger and older offspring, the relationship between parental MH and offspring suicide remained significant only for those aged under 24 years. Few studies have examined the impact of parental psychopathology across sensitive life periods in children and adolescents, but this finding, together with those of Niederkotenthaler et al. (Niederkrotenthaler et al., Reference Niederkrotenthaler, Floderus, Alexanderson, Rasmussen and Mittendorfer-Rutz2012) support the hypothesis that early exposure to parental psychopathology during neuro-developmentally sensitive periods may increase risk of suicide. It is also plausible that the impact of environmental influences, including parental psychopathology, on offspring MH and suicidality may decrease with increasing age and independence from the family unit. It is also important to note that these older individuals may have moved out of the family home during follow-up, therefore lessening the observed parental-offspring associations. However, given that the confidence intervals were wide and cross unity, this observation may be the result of insufficient statistical power to detect the true association between the number of parents who reported poor MH and suicide risk among offspring aged 24+ years.

Studies suggest that the risk of suicide varies according to the parent affected. A recent systematic review concluded that the risk of SRBs and death by suicide in children was higher when it was the mother rather than the father who had poor MH though, for death by suicide alone the evidence for a differential impact of parental sex was less conclusive (Goodday et al., Reference Goodday, Shuldiner, Bondy and Rhodes2019). In two case–control studies using national registers in Denmark, maternal psychiatric hospitalisation was associated with a minimally increased risk of offspring suicide compared to those with a record of paternal psychiatric hospitalisation(Webb et al., Reference Webb, Pickles, Appleby, Mortensen and Abel2007; Stenager and Qin, Reference Stenager and Qin2008), and in a Swedish population-based case–control study, maternal schizophrenia was associated with slightly higher odds of offspring suicide than paternal schizophrenia (Ljung et al., Reference Ljung, Lichtenstein, Sandin, D'Onofrio, Runeson, Långström and Larsson2013). However, it is unclear whether the differential risk estimates observed in these studies were statistically significantly different. The current study does not resolve the issue. The elevated risk of offspring with poor MH was marginally greater for individuals living with a mother with poor MH, but conversely, the risk of offspring suicide was greater to in those living with a father with poor MH. Previous research on parenting and child psychopathology suggests that although the quality of paternal-child relationships strongly predicts the emotional and behavioural outcomes of offspring, the impact of maternal influence supersedes that of the father, presumably as the primary burden of parental care is adopted by the mother (Flouri, Reference Flouri2010).

Strengths and limitations

This population-wide cohort study provided a unique opportunity to examine the relationship between parental MH and offspring psychopathology and suicide risk in a typically hard to reach population. The self-reported indicator of poor MH encompassed a wider range of psychopathology than studies based on admission to a psychiatric hospital, making these findings more generalisable to the wider body of individuals with mental ill-health. Although admission data has the benefit of high specificity, it excludes the much larger proportion of psychiatric ill-health that is managed in the community. Additionally, population surveys which use validated diagnostic instruments, though arguably the most accurate measurement of MH, are resource intensive, require a clinical application or specialist interviewer training and cannot cover more than a small proportion of the population. However, as the Census measure used included only those with conditions that had or were expected to last at least twelve months, people with less protracted episodes of poor MH will not have been included. Furthermore, a self-report measure, while democratising the identification process, is subject to reporting bias especially related to the continuing stigma surrounding mental illness. However, this indicator has face validity based on its demographic distribution which mirrors known associations with MH, correlational validity as it is associated with receipt of psychotropic medication, and predictive validity as it is a strong predictor of death by suicide (Tseliou et al., Reference Tseliou, Maguire, Donnelly and O'Reilly2015; Rosato et al., Reference Rosato, Tseliou and O'Reilly2019; Onyeka et al., Reference Onyeka, O'Reilly and Maguire2021).

As parental and offspring MH were measured at the same time point, establishing causal order by accounting for reverse causality was not possible. There is likely some degree of bidirectionality to this association, however, the association persisted with adjustment for person MH status, and only 1.62% of children reported poor MH despite 11.6% living with an affected parent, providing some indication of the direction of the association. This also limited the statistical modelling to logistic regression, however, there is an argument that when the outcome is rare and the follow-up period is short, the regression coefficients obtained through logistic regression approximate those obtained through Cox regression (Green and Symons, Reference Green and Symons1983; Ingram and Kleinman, Reference Ingram and Kleinman1989; Ingram et al., Reference Ingram, Kleinman and Mock1990). Finally, while Census-based studies provide population coverage, they lack depth and additional information on important household factors, such as substance dependencies in parents or exposure to adverse childhood experiences which would have contributed to our understanding of factors that may mediate these associations. Owing to the study design, it was not possible to examine the extent to which the observed parent-offspring associations could be explained by shared genetic factors. As such, further investigation into the mechanisms underpinning these associations is warranted.