Violence, Adversity, and Children's Distress: The Interplay of Genotype and Social Responses

Children are subjected to violence or witness violence by family members at epidemic rates. In a quest to understand children's suffering when exposed to violence, recent research has linked the genotypes of maltreated children with measures of their distress and aggression. Indeed, some researchers suggest children's resilience to adversity is dependent on their genotypes. This view conceals the importance of social responses, encourages the pathologizing of children who show distress and aggression, and suggests these children are less likely to benefit from therapy or other constructive social responses. However an alternative analysis of the research points to very different and more optimistic conclusions. In this paper, I critically review recent research on the role of genotype in maltreated children's distress and aggression and show that it supports the more contextual view that certain genes may contribute to greater responsiveness to both adversity and social support. I outline the significance of this analysis for contesting biological determinism and for providing effective social responses to children who witness or endure violence.

For the past few centuries in the Western World, the quest for understanding of human suffering has concentrated on a search for biological aetiologies. This has led to research in recent decades into possible genetic causes of mental and emotional distress. However, situating the source of human distress in the genome has profound implications for social policy and professional practice. Interventions are focused on treating individuals, while relationships between social problems and emotional distress are concealed: "The individual becomes a problem for society to cope with rather than society becoming a problem for the individual" (Lewontin, 1991, p. 16). The message is, "You have no control. It's in the genes" (Borges, 1995, p. 225). Such a view serves to legitimate the social status quo.

Having failed to find any direct "X is a gene for Y" (Kendler, 2005, p. 1243) relationships for emotional distress however, geneticists have turned their attention to gene-environment (G x E) interactions. Researchers now propose that "differences between individuals, originating in the DNA sequence, bring about differences between individuals in their resilience or vulnerability to the environmental causes of many pathological conditions of the mind and body" (Caspi & Moffitt, 2006, p. 584). Thus we find in the literature terms such as "most vulnerable genotypes" (Kaufman, 2008, p. 152) and "genetic vulnerability" (Caspi & Moffitt, 2006, p. 588). While this view acknowledges some role for environment, it still places the source of human distress within the individual by suggesting a deficiency associated with certain genotypes. Thus the focus is still on treating individuals, perhaps by changing their biology through the use of medication, while the roles of social problems and supportive social responses continue to receive minimal attention.

Recent research examining different variations (alleles) of the serotonin transporter (5-HTT) gene shows that children with two short alleles (s/s) of the gene are likely to experience greater distress when exposed to adversity than children with one or two long alleles (s/l or l/l) (Capsi et al., 2003; Eley et al., 2004; Kaufman et al., 2004, 2006). However, among study participants who were not maltreated, those with the s/s genotype experienced levels of distress that were similar to (Kaufman et al., 2004, 2006) or lower than (Caspi et al, 2003; Eley et al., 2004) distress levels of those with s/l or l/l genotypes. Furthermore, maltreated children with the s/s genotype were also more responsive to social support than maltreated children with s/l or l/l genotypes (Kaufman et al., 2004, 2006). In fact, Kaufman et al. (2006) found that depression scores of maltreated children with two short alleles who received low levels of social support were twice as high as those of maltreated children with the same genotype who received high levels of social support, and depression scores of the latter group were only slightly higher than those of children in the control group.

Eley et al. (2004) studied girls ages 12 – 19 who scored in either the top or bottom 15% of an initial sample of participants who completed the Mood and Feelings Questionnaire. Girls with the s/s genotype who were in the low environmental risk group were more likely to be in the low depression scores group. Those with the s/s genotype who were in the high environmental risk group were more likely to be in the high depression scores group. Girls with the s/l or l/l genotypes were more likely to be in the high depression scores group regardless of environment. While 79% of girls with the s/s genotype and high environmental risk were in the high depression scores group, it is notable that the remaining 21% were in the low depression scores group. This suggests that outcomes of gene-environment interactions were neither predetermined nor predictable based on the girls' 5-HTT genotype and are perhaps better described in terms of probabilities.

The biological mechanisms of responses associated with the short 5-HTT allele have evaded elucidation and appear to be paradoxical as the short allele is associated with decreased activity of the serotonin reuptake transporter, "precisely the functional effect of the SSRIs used to treat depression" (Mill & Petronis, 2007, p. 801).

While the long allele of the serotonin transporter gene is portrayed as conveying resilience to adversity when measured in terms of depression scores, it is also associated with higher baseline blood pressure levels; greater cardiovascular reactivity (CVR) i.e., greater increases in blood pressure and heart rate in response to stress; and higher rates of cardiovascular disease (CVD) (Williams et al., 2008). How then do we measure "vulnerability" and "resilience," by depression scores, by responses to social support, by CVR and CVD, or by other measures?

Males as young as seven years old who have a low-activity allele of the monoamine oxidase A (MAOA) gene have been shown to be more likely to display higher levels of distress and aggression after being subjected to physical abuse than those with a high-activity allele of the gene (Caspi et al, 2002; Kim-Cohen et al., 2006). (This research was conducted exclusively with males as the MAOA gene is situated only on the X chromosome and males therefore have only one MAOA allele.) When there was no history of physical abuse however, males with a low-activity MAOA allele were less likely to be aggressive than those with a high-activity MAOA allele. Kim-Cohen et al. found that "boys with the genotype conferring high MAOA activity had slightly but significantly elevated levels of global mental health problems as well as antisocial behavior and attention-deficits/hyperactivity relative to boys with the low-activity genotype" (p. 910). Thus low-activity MAOA alleles are associated with lower aggression levels in the absence of physical abuse and higher aggression levels in the presence of physical abuse. The reverse associations are seen for the high activity alleles. Which allele is associated with increased "vulnerability" appears to vary depending on the presence or absence of physical abuse.

How are gene-environment interactions mediated? While specific mechanisms for actions associated with the short 5-HTT allele and low-activity MAOA alleles remain elusive, recent research shows there is an ongoing dynamic interplay between genes and environment, mediated by what are called epigenetic (control above genetics) factors. These factors direct the expression of genes in response to circumstances and situations of people's lives (Bredy et al., 2004; Fraga et al., 2005; Lipton, 2005; Mill & Petronis, 2007; Szyf, Weaver, & Meaney, 2007; Weaver et al., 2004).

"DNA is wrapped around a protein-based structure termed chromatin . . . which is formed of . . . histone proteins" (Szyf et al., 2007, p. 10). "The N-terminal tails of these histones are extensively modified by methylation, phosphorylation, acetylation . . . The state of modification of these tails plays an important role in defining the accessibility of the DNA" (Szyf et al., p. 10).

DNA methylation is a process by which methyl groups attach to promoter regions of genes, preventing expression of the related genes (Mill & Petronis, p. 803). Epigenetic markers are very fluid, responsive to the environment, and changeable over the course of a lifetime. (Fraga et al., 2005). Genes are not self-propagating. Their expression is intricately managed by complex cellular systems in response to the environment.

Discussion

The above-mentioned research suggests that rather than characterizing the short allele of the serotonin transporter gene and the low-activity alleles of the MAOA gene as conveying genetic vulnerability, a more accurate view may be that these alleles contribute to greater responsiveness to environment: People with these alleles may experience greater distress in response to adversity and may also respond more positively to social support and in fact thrive in supportive environments. Thus, rather than considering human distress and aggression as genetically determined and therefore unlikely to respond to positive social interventions, this research suggests a likelihood that the opposite conclusion may be valid i.e., those who show the greatest distress or aggression in response to adversity may also be most likely to respond positively to social support. This has significant implications for therapeutic practice. We might compare a contextualized and supportive approach with current common practices of reducing social support for those who commit crimes. We might examine ways of reducing common negative social responses to victims of crime and ways of enhancing positive social responses.

This research also demonstrates a significant relationship between research results and research design: Results are dependent on what is measured e.g., depression scores or CVR. (See table 1.) In order to further elucidate gene-environment interactions, it appears necessary to consider a wider variety of environments and human responses.

Table 1 - Measures of s/s 5-HTT genotype by environment interactions