16b
Marina A. Bornovalova, Alexandria M. Choate, and Haya Fatimah
The last 20 years have seen substantial advances in estimating genetic/temperamental and environmental contributions to the development and maintenance of borderline personality disorder (BPD). Stressful life events (SLEs) and other environmental contributions to BPD have been studied extensively and the importance of these SLEs is captured quite well in the chapter by Crowell, Kaliush, and Vlisides-Henry (this volume). However, the transactions which are reciprocal effects between the person and his or her environment are empirically overlooked despite the fact that such transactions are at the heart of many theories of psychopathology. In this commentary, we argue that a look at the broader personality and psychopathology literature suggests indirect evidence for transactional mechanisms in BPD and the important role transactional processes play in the development and maintenance of the disorder.
Studies of Child and Adolescent Factors: Etiological Transactional Processes
Environmental events are not entirely environmental. Studies of BPD etiology and maintenance traditionally separate personal (temperamental, genetic) and environmental (trauma, stressful life events, parenting factors) into two distinct “boxes.” Environmental factors contributing to BPD include (but are not limited to): trauma, stressful life events (SLEs), and parenting styles – especially punishment (lack of), warmth, negativity, and control (Schuppert, Albers, Minderaa, Emmelkamp, & Nauta, 2012). However, studies using the classical twin design report that these putatively environmental factors show at least partial genetic contribution. For example, Kendler and Baker (2007) conducted a systematic review of genetic influences on environmental factors and found parenting to be largely heritable, with heritability estimates highest for parental warmth (34–37 percent), and lower for measures of control and negativity (12–17 percent). Family environment (support, cohesion, expressiveness, control, independence) was also 18–30 percent heritable. This general pattern held regardless of whether the child or parent reported on parenting behavior. On the other hand, childhood trauma – another correlate of BPD – does not seem to be particularly heritable; there is at best very modest heritability for emotional abuse, and little to no heritability of physical and sexual abuse (Bornovalova et al., 2013; Jaffee et al., 2004; but see Richmond-Rakerd et al., 2019 and Schaefer et al., 2018 for converse findings).
Generally, the heritability of environmental factors suggests both active and evocative gene–environment correlations (Scarr & McCartney, 1983). These correlations are direct analogs of the transactional processes in BPD. Evocative gene–environment correlations (rGE) result from the environment (e.g., parenting) differentially responding to genetically influenced characteristics of the child. Evocative rGE captures a transactional process between offspring and their parents: for instance, parents may respond to the child’s difficult temperament with harsh and negative parenting. Conversely, active rGE occurs when a child actively selects environments that are correlated with his or her genetically influenced characteristics (“niche-picking”); active rGE is less relevant to transactions with parents, but is relevant to the general adolescent social context (e.g., peer selection).
Personality likely contributes to the heritability of parenting in BPD. One way to unpack processes driving rGE is to examine the genetic correlation of the environmental variable of interest (e.g., parenting) and another variable (e.g., BPD, normal personality traits. No studies yet document the genetic correlation between BPD traits and parenting factors, but the normal personality literature is informative. Krueger, Markon, and Bouchard (2003) reported a small phenotypic (~.16) but large genetic (.77) correlation between personality traits of negative emotionality and retrospectively reported parental acceptance, conflict, and control. The genetic correlation between the trait-constraint (impulsivity reversed) and parenting was .64.
Non-twin longitudinal studies directly provide evidence for the offspring’s personality contributions to parenting. Whalen et al. (2014) coded transactions between mothers and daughters in the laboratory and found dyadic negative escalation to be predictive of increased BPD symptoms over time. Similar effects were found in a study of children and their biological mothers suggesting maladaptive mother–child interactions mediate the longitudinal transmission of maternal BPD symptoms to their offspring (Reinelt et al., 2014). Finally, a large longitudinal study examined the developmental trajectories of BPD symptoms in relation to parenting. Time-specific elevations in BPD symptoms predicted increases in harsh punishment and low warmth (but not vice versa). Child impulsivity and negative emotionality as well as caregiver psychopathology predicted parenting trajectories, whereas only child characteristics were predictive of BPD trajectories (Stepp et al., 2014).
Personality may mediate the relationship between BPD and heritable non-family social experiences. We know little about the non-family social context of children and adolescents with BPD features. Yet, although the biosocial models do not explicitly describe the social lives of adolescents at risk for BPD, one would expect that patterns developed in the context of the family would partially translate into non-family contexts. Notably, number of friends, social support, and bullying are moderately to highly heritable in adolescence (Bowes et al., 2013) and show genetic correlations with personality and psychopathology. For instance, Connolly and Beaver (2016) found the heritability of bullying victimization to be ~70 percent. Bullying victimization correlated with child delinquency and child depression/anxiety, and common genetic factors partially mediated these relationships. In a sample of late adolescents, Billig, Hershberger, Iacono, and McGue (1996) reported trait-constraint to have a high genetic correlation (.69) with non-independent/non-family SLEs. Non-twin studies provide support as well: Jensen-Campbell et al. (2002) reported that neuroticism was correlated with perceived peer acceptance, whereas agreeableness was significantly associated with peer-reported acceptance and friendship.
Studies of Adult Factors: Maintenance/Exacerbation Transactional Processes
Development and maintenance of BPD do not end in adolescence, and neither do the transactions between the person and his or her environment. New pathogenic or maintenance factors are also possible and are implicitly predicted by the biosocial model. For instance, the model makes predictions regarding the carry-over effects of patterns learned and reinforced in childhood into interpersonal, romantic, and social relationships. It likewise makes predictions for lifestyle choices that increase the probability of experiencing stressful life events. Fortunately, the literature describing how BPD actively transacts with its environment in adulthood is slowly accumulating.
BPD is associated with social difficulties and stressful life events in adulthood. While BPD symptoms are associated with a range of negative outcomes, these effects may not be specific to BPD. In a four-year longitudinal study, Daley, Burge, and Hammen (2000) reported that BPD symptoms predicted four-year romantic dysfunction (e.g., romantic chronic stress, conflicts, partner satisfaction, abuse, and unwanted pregnancy), and less partner-reported satisfaction. However, these associations were not unique to BPD, but accounted for by general personality pathology. SLEs also appear to be correlated with BPD features: in two studies of middle-aged adults, BPD features predicted negative life events – especially dependent and interpersonal life events – even after adjusting for depression and other personality disorders (Gleason, Powers, & Oltmanns, 2012; Powers, Gleason, & Oltmanns, 2013).
Adult environmental events are also heritable. Numerous twin studies have documented the contribution of active and evocative gene–environment correlations to life events common to those with BPD including marital difficulties, divorce, SLEs, and trauma in adulthood. Divorce shows a weighted mean heritability of 35 percent, with heritability of marital satisfaction, conflict, and warmth ranging from 13 percent for conflict to 28 percent for satisfaction (Kendler & Baker, 2007). Personality characteristics of negative emotionality, constraint, aggression, positive emotionality, and optimism have significant genetic correlations with divorce and marital problems in the expected direction (Chipuer, Plomin, Pedersen, McClearn, & Nesselroade, 1993; Jocklin, McGue, & Lykken, 1996; Spotts et al., 2005). SLEs appear to be similarly heritable (17–31 percent), with reporting of high-risk (62 percent) and military trauma (47 percent) demonstrating genetic contributions as well (Kendler & Baker, 2007; Lyons et al., 1993; Richmond-Rakerd et al., 2019).
Personality contributes to heritable adult life events. In a large longitudinal twin study, genetic factors were found to partially contribute to negative controllable and less controllable life events, though the majority of this contribution was environmental (Kandler, Bleidorn, Riemann, Angleitner, & Spinath, 2012). Neuroticism and agreeableness had a moderate, genetically mediated effect on future SLEs, whereas the effects from life events on personality were environmentally mediated. Evidence from molecular data also provide evidence for genetic influences on adverse life experiences: 30 percent of variance in reported SLEs including dependent (illness, death, and being robbed) – and independent (unemployment, separation, financial problems, and legal matters) – life events were explained by single nucleotide polymorphisms (SNPs). When traits of neuroticism and behavioral disinhibition were ruled out, genetic contributions to SLEs disappeared (Powers et al., 2013).
Working Theoretical Model: Genetic Control of Exposure to the Environment in BPD
Kendler and Eaves (1986) describe a model of depression – termed “genetic control over exposure to the environment” – that may be useful for testing person–environment transactions in BPD over the lifespan. This model posits that genes can act on the liability to psychiatric illness by predisposing individuals to select themselves into high-risk environments. Kendler, Karkowski, and Prescott (1999) documented that relative to individuals without a history of depression, individuals with depressive disorders experience more SLEs. These events are at least partially dependent on one’s genetic liability. Hammen (2006) and Joiner (2000) suggest processes by which individuals with depression generate interpersonal and dependent life events. These include poor interpersonal problem-solving, negative feedback and excessive reassurance seeking, interpersonal conflict avoidance, and blame maintenance. Although genetic control over environmental exposure is nested within the biosocial theory, there are benefits for model multiplication. First, invoking Kendler and Eaves’ model places BPD in the context of general psychopathology and invites tests of whether effects are specific to BPD. Second, this model provides a well-developed body of methodological and empirical literature using both phenotypic and genetically informative designs. This literature can then serve as a metaphorical trail of breadcrumbs for tests of the same phenomena in BPD.
We extend this model to BPD by positing that (i) the traits of neuroticism, agreeableness, and conscientiousness at least partially mediate the relationship of BPD with the experience of negative parenting, interpersonal stress, and SLEs, and this mediation is genetic in origin. In childhood and adolescence, BPD – partially through these traits – contributes to environmental stressors (e.g., experience of being bullied), as well as reduced parental warmth and increased negativity. In adulthood, these traits contribute to increased exposure to interpersonal and dependent life events. (ii) This transactional process continues to develop throughout the lifespan with different trait combinations contributing to a wide array of social processes such peers vs. family influence. (iii) The effects of the person on the environment may not be specific to BPD, but instead may be indicative of a general liability to interpersonal, personality, and affective dysfunction.
Future Directions
Many gaps remain in our understanding of transactional processes in BPD across the lifespan. Foremost, there is a clear need for direct tests of BPD and its transactions with the environment – and the mechanisms driving those transactions. These transactions should be studied outside as well as within the family and throughout the lifespan. It is important to note that personality disorders – especially when conceptualized as an extensions of normal personality – are likely to be polygenic, and candidate gene studies are unlikely to be fruitful. For now, researchers studying the genetic basis of BPD would be best served by using existing twin and adoptive datasets or genome-wide association studies from very large data sets. Multi-morbidity should be modeled in molecular studies as well. Such questions can be examined within existing longitudinal and/or genetically informative epidemiological studies that routinely collect data on normal personality traits. These normal personality traits can be subsequently scored to provide a proxy of BPD features. Finally, given evidence for the direct effects of adverse environments on BPD features, detection of the individual-based contributing factors to environmental exposure can aid prevention efforts that can target these malleable traits. In turn, this may reduce the risk of environmental stressor exposure in vulnerable individuals.
References
Billig, J. P., Hershberger, S. L., Iacono, W. G., & McGue, M. (1996). Life events and personality in late adolescence: Genetic and environmental relations. Behavior Genetics, 26(6), 543–554.
Bornovalova, M. A., Huibregtse, B. M., Hicks, B. M., Keyes, M., McGue, M., & Iacono, W. (2013). Tests of a direct effect of childhood abuse on adult borderline personality disorder traits: A longitudinal discordant twin design. Journal of Abnormal Psychology, 122(1), 180–194.
Bowes, L., Maughan, B., Ball, H., Shakoor, S., Ouellet-Morin, I., Caspi, A., … Arseneault, L. (2013). Chronic bullying victimization across school transitions: The role of genetic and environmental influences. Development and Psychopathology, 25(2), 333–346.
Chipuer, H., Plomin, R., Pedersen, N. L., McClearn, G. E., & Nesselroade, J. R. (1993). Genetic influence on family environment: The role of personality. Developmental Psychology, 29(1), 110–118.
Connolly, E. J., & Beaver, K. M. (2016). Considering the genetic and environmental overlap between bullying victimization, delinquency, and symptoms of depression/anxiety. Journal of Interpersonal Violence, 31(7), 1230–1256.
Daley, S. E., Burge, D., & Hammen, C. (2000). Borderline personality disorder symptoms as predictors of 4-year romantic relationship dysfunction in young women: Addressing issues of specificity. Journal of Abnormal Psychology, 109(3), 451–460.
Gleason, M. E., Powers, A. D., & Oltmanns, T. F. (2012). The enduring impact of borderline personality pathology: Risk for threatening life events in later middle-age. Journal of Abnormal Psychology, 121(2), 447–457.
Hammen, C. (2006). Stress generation in depression: Reflections on origins, research, and future directions. Journal of Clinical Psychology, 62(9), 1065–1082.
Jaffee, S. R., Caspi, A., Moffitt, T. E., Polo-Tomas, M., Price, T. S., & Taylor, A. (2004). The limits of child effects: Evidence for genetically mediated child effects on corporal punishment but not on physical maltreatment. Developmental Psychology, 40(6), 1047–1058.
Jensen-Campbell, L. A., Adams, R., Perry, D. G., Workman, K. A., Furdella, J. Q., & Egan, S. K. (2002). Agreeableness, extraversion, and peer relations in early adolescence: Winning friends and deflecting aggression. Journal of Research in Personality, 36(3), 224–251.
Jocklin, V., McGue, M., & Lykken, D. T. (1996). Personality and divorce: A genetic analysis. Journal of Personality and Social Psychology, 71(2), 288–299.
Joiner Jr, T. E. (2000). Depression’s vicious scree: Self‐propagating and erosive processes in depression chronicity. Clinical Psychology: Science and Practice, 7(2), 203–218.
Kandler, C., Bleidorn, W., Riemann, R., Angleitner, A., & Spinath, F. M. (2012). Life events as environmental states and genetic traits and the role of personality: A longitudinal twin study. Behavior Genetics, 42(1), 57–72.
Kendler, K. S., & Baker, J. H. (2007). Genetic influences on measures of the environment: A systematic review. Psychological Medicine, 37(5), 615–626.
Kendler, K. S., & Eaves, L. J. (1986). Models for the joint effect of genotype and environment on liability to psychiatric illness. American Journal of Psychiatry, 143(3), 279–289.
Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between stressful life events and the onset of major depression. American Journal of Psychiatry, 156(6), 837–841.
Krueger, R. F., Markon, K. E., & Bouchard Jr, T. J. (2003). The extended genotype: The heritability of personality accounts for the heritability of recalled family environments in twins reared apart. Journal of Personality, 71(5), 809–833.
Lyons, M. J., Goldberg, J., Eisen, S. A., True, W., Tsuang, M. T., Meyer, J. M., & Henderson, W. G. (1993). Do genes influence exposure to trauma? A twin study of combat. American Journal of Medical Genetics, 48(1), 22–27.
Powers, A. D., Gleason, M. E., & Oltmanns, T. F. (2013). Symptoms of borderline personality disorder predict interpersonal (but not independent) stressful life events in a community sample of older adults. Journal of Abnormal Psychology, 122(2), 469–474.
Reinelt, E., Stopsack, M., Aldinger, M., Ulrich, I., Grabe, H. J., & Barnow, S. (2014). Longitudinal transmission pathways of borderline personality disorder symptoms: From mother to child? Psychopathology, 47(1), 10–16.
Richmond-Rakerd, L. S., Trull, T. J., Gizer, I. R., McLaughlin, K., Scheiderer, E. M., Nelson, E. C., … Heath, A. C. (2019). Common genetic contributions to high-risk trauma exposure and self-injurious thoughts and behaviors. Psychological Medicine, 49(3), 421–430.
Scarr, S., & McCartney, K. (1983). How people make their own environments: A theory of genotype→ environment effects. Child Development, 54(2), 424–435.
Schaefer, J. D., Moffitt, T. E., Arseneault, L., Danese, A., Fisher, H. L., Houts, R., … Caspi, A. (2018). Adolescent victimization and early-adult psychopathology: Approaching causal inference using a longitudinal twin study to rule out noncausal explanations. Clinical Psychological Science, 6(3), 352–371.
Schuppert, H. M., Albers, C. J., Minderaa, R. B., Emmelkamp, P. M., & Nauta, M. H. (2012). Parental rearing and psychopathology in mothers of adolescents with and without borderline personality symptoms. Child and Adolescent Psychiatry and Mental Health, 6(1), 29.
Spotts, E. L., Lichtenstein, P., Pedersen, N., Neiderhiser, J. M., Hansson, K., Cederblad, M., & Reiss, D. (2005). Personality and marital satisfaction: A behavioural genetic analysis. European Journal of Personality, 19(3), 205–227.
Stepp, S. D., Whalen, D. J., Scott, L. N., Zalewski, M., Loeber, R., & Hipwell, A. E. (2014). Reciprocal effects of parenting and borderline personality disorder symptoms in adolescent girls. Development and Psychopathology, 26(2), 361–378.
Whalen, D. J., Scott, L. N., Jakubowski, K. P., McMakin, D. L., Hipwell, A. E., Silk, J. S., & Stepp, S. D. (2014). Affective behavior during mother–daughter conflict and borderline personality disorder severity across adolescence. Personality Disorders: Theory, Research, and Treatment, 5(1), 88–96.
This work was supported by DA032582 (NIDA). No conflict of interest exists for any of the authors