The adoption of children is a fundamental method of building families. However, adoptees may face subsequent adaptive challenges associated with family stress at the time of birth and during the adoption process.
It should be no surprise, then, that adoptees have a small but well-known increased risk for depression, anxiety and other mental health disorders.
The health effect has been attributed to stressful early childhoods. But genetics also plays a role, according to a large new study published in Biological Psychiatry, published by Elsevier.
“We found adopted individuals on average had a somewhat higher genetic risk for mental health problems, but the effects are quite small,” said lead author Kelli Lehto, PhD, a postdoctoral researcher at Karolinska Institute in Stockholm. “Overall, the main message here is that both environment and genetics are important.”
Psychiatric disorders, including depression, anxiety and schizophrenia are, to varying degrees, heritable. Genome-wide association studies (GWAS) have identified a growing number of genetic markers associated with the risk for most major psychiatric disorders so that a ‘polygenic risk score’ for these disorders may be estimated.
Dr. Lehto and colleagues analyzed the genomic and health information data of 243,797 participants in the UK Biobank, a major health resource established by the Wellcome Trust and others, including a group of 3,151 who were adopted as children within Britain, mostly in the 1950s and 1960s.
Overall, the adoptees in the study reported being happy and satisfied with their lives. When compared to the general population, they were more likely to be male, to smoke, have less education, attain a lower income, and to experience more stressful life events.
Adoptees also had slightly more mental health problems, such as depressive symptoms, bipolar disorder, higher neuroticism and loneliness.
The researchers found a slightly elevated genetic risk of depression, schizophrenia and neuroticism among adoptees.
They did not find however, any evidence of interaction between genetics and adoption on mental health.
Thus, while children put up for adoption were at increased genetic risk for developing symptoms of mental illness, the adoption process did not appear to increase the impact of this genetic risk.
“Basically, genetic risk and adoption each are predictors of psychiatric problems,” explained Dr. Lehto. “It’s important to highlight that adoption and genetic risk each only contributed a small amount to the individual differences in mental health.
That indicates many more factors contribute to the development of mental health problems.”
Psychiatric disorders, including depression, anxiety and schizophrenia are, to varying degrees, heritable. Image is in the public domain.
“There are many complicated issues to consider in these findings,” John Krystal, MD, Editor of Biological Psychiatry.
“But the most straightforward implication is that adopted children may face both special environmental and genetic risks for adjustment problems and mental illness.
Awareness of these risks increases the importance of programs aimed at early detection and intervention for these children.”
The findings of this study of people with UK-based ancestry pertain only to people of European ancestry and the results might be different in other groups. Scientists note significant racial and ethnic differences in the findings from genome-wide association studies (GWAS).
“It would be important to study resilience factors as well as risk factors, Dr. Lehto said.
“The differences between adoptees and the rest of the population are very small. Generally, adoptees are doing well.” The findings may apply to other types of childhood adversity and adult mental health outcomes among non-adoptees, she added.
It is well established that anxiety disorders run in families, with strong evidence for associations between parent and child anxiety (Lawrence, Murayama, & Creswell, 2018; Micco et al., 2009; Sydsjo, Agnafors, Bladh, & Josefsson, 2018).
However, the mechanisms underlying these associations remain unclear. Children of anxious parents can inherit genes associated with the development of anxiety from their parents (a genetic mechanism); anxious parents and children can behave in ways that promote anxiety in the other (environmental mechanisms); and negative environments shared by both generations can simultaneously influence anxiety in both.
These mechanisms are not mutually exclusive. To better understand intergenerational anxiety associations in families, researchers should explore multiple mechanisms concurrently, requiring the use of genetically informed, longitudinal research.
Traditional twin studies suggest that childhood anxiety symptoms are moderately heritable (Boomsma, Van Beijsterveldt, & Hudziak, 2005; Trzaskowski, Zavos, Haworth, Plomin, & Eley, 2012).
This infers that around half of the individual differences in vulnerability to anxiety can be explained by environmental influences, and half by genetics. When parents and children are genetically related, it follows that any parent–child anxiety correlation might be influenced by shared genes. Researchers have used a cross‐sectional children‐of‐twins design to directly examine genetic mechanisms influencing intergenerational anxiety associations (Eley et al., 2015).
Here, the correlation between parent and adolescent anxiety was not significantly confounded by genetic relatedness, indicating that the familial association could be attributable to environmental exposure to an anxious relative.
However, it was not possible to identify the direction of effects between generations. Environmental parent‐to‐child anxiety transmission may occur as a result of maladaptive parenting and/or child observational and instruction‐based learning (Aktar, Nikolić, & Bögels, 2017; Ginsburg & Schlossberg, 2002).
Researchers have focussed particularly on the role of parent over‐involvement (Aktar et al., 2017; Eley, Napolitano, Lau, & Gregory, 2010; Ginsburg & Schlossberg, 2002; Hudson, Comer, & Kendall, 2008; Murray, Creswell, & Cooper, 2009). Less attention has been paid to theoretical models of development which posit that intergenerational associations may be transactional (Bell, 1968).
Child‐to‐parent anxiety effects have seldom been assessed. Therefore, whilst research indicates that the environment plays a significant part in the familial transmission of anxiety, our understanding of the underlying mechanisms remains limited.
To examine transactional associations between parents and children, we require longitudinal studies that enable parent‐to‐child and child‐to‐parent effects to be assessed simultaneously. The first genetically informed research on transactional effects between parent anxiety and child outcomes was conducted using the same prospective adoption sample as in the present manuscript; the Early Growth and Development Study (EGDS; Brooker et al., 2015).
In the adoption design, adoptive parent and child associations are free from confounding by genetic relatedness. When children are adopted at birth to nonrelatives, as in the EGDS, birth parent and child associations act as a proxy measure of inherited genetic effects.
Focussing on infant offspring in the EGDS sample, results demonstrated both parent‐to‐child and child‐to‐parent effects between adoptive parent anxiety symptoms and infant negative affect (Brooker et al., 2015).
Like Eley et al. (2015), no evidence was found for genetic parent–child associations, using birth parent negative affect to model genetic transmission. In other samples, it has been suggested that child anxiety elicits ‘extreme control’ in mothers, with both phenotypes influenced by the child’s genetic makeup (Eley et al., 2010); and mothers of clinically anxious children respond to child negative affect with greater intrusive involvement than mothers of nonanxious children (Hudson et al., 2008).
Given the focus on mother–child dyads in the existing literature, there are now growing efforts to investigate the role of fathers as well. A direct influence of paternal depression on offspring mental health has been reported in several (Class et al., 2012; Lewis, Neary, Polek, Flouri, & Lewis, 2017; Pemberton et al., 2010; Ramchandani et al., 2008) but not all (Tully, Iacono, & McGue, 2008) studies including fathers, which were not all genetically informed.
Father–child anxiety associations have been seldom studied. Researchers suggest that mothers’ and fathers’ anxiety and behaviour may be differentially associated with offspring anxiety across development, with the father’s role increasing over time (Connell & Goodman, 2002; Hudson et al., 2008; Moller, Majdandzic, & Bogels, 2015; Weijers, van Steensel, & Bögels, 2018).
Evolutionary theory suggests that fathers encourage offspring to confront the external world, and children look more to fathers in threatening situations for clues on how to respond. Anxious fathers may not fulfil these roles, thereby influencing the development of child anxiety (Bögels & Perotti, 2011; Bögels & Phares, 2008; Paquette, 2004).
Furthermore, as fathers typically adopt fewer care‐giving responsibilities than mothers, they may be less susceptible to the emotional impact of offspring psychopathology (Bögels & Perotti, 2011; Weijers et al., 2018).
Ideally, researchers should examine the role of both parents together, considering how all three individuals influence one another’s mental health (Davies & Cicchetti, 2004). Such work should assess whether previously reported dyadic parent–child anxiety associations remain significant in mother–father–child analyses, which better reflect the social and genetic nature of most families.
We used the EGDS adoption sample to conduct the first study of transactional associations between parent and child anxiety symptoms during middle childhood. We follow‐up on previous research showing that intergenerational anxiety associations between adolescent offspring and parents are under environmental influence (Eley et al., 2015).
We expected to find similar results during middle childhood when anxiety disorders first begin to develop, whilst expanding on this to explore transactional intergenerational effects. We used age‐appropriate anxiety measures in each generation, with two parents reporting on child anxiety. We controlled for passive genetic effects by examining children who were adopted at birth, and we explored the role of inherited effects using a composite measure of lifetime internalising problems among birth parents and their first‐degree relatives.
This composite was designed to reflect a single internalising liability factor, capturing multiple internalising symptoms and diagnoses across time, based on evidence for their strong genetic overlap and that persistent problems are under greater genetic influence (Caspi et al., 2014; Kendler et al., 2011; Krueger & Markon, 2006; Waszczuk, Zavos, Gregory, & Eley, 2014).
We sought to understand whether lifetime risk reported in adulthood was associated with genetically influenced symptoms in biological offspring (Boomsma et al., 2005). We included birth parent, adoptive mother, father and child symptoms together in longitudinal models. We expected that results would differ by parent gender, but no further expectations were made as this is the first genetically informed, longitudinal study of transactional intergenerational anxiety associations.