As in all aspects of child psychiatry, a developmental perspective is crucial when considering environmental risks. Some developmental periods may be especially sensitive for neurodevelopment, and show heightened effects of environmental insults. In addition, key sources of environmental influence change with age, and the meaning and impact of events will vary with the child’s stage of cognitive, emotional, and social development. The family is the central source of early environmental influences, charged as it is in most societies with prime responsibility for the care, nurture, and socialization of the young. As children develop, so their social worlds expand; childcare and school settings take on increased importance, as do relationships with friends and peers. Throughout, each of these proximal contexts is shaped by influences from the wider culture and society. Any comprehensive assessment of a child’s environment needs to take each of these types and levels of influence into account.

At one time, causal associations between adverse experiences and childhood disorder were assumed to run in just one direction. Today, it is clear that the situation is vastly more complex. Children are not simply passive recipients of experience; they influence, as well as being influenced by, those around them, and they play an active role in constructing and interpreting their social worlds.⁽¹⁾ Even very young infants influence the nature of their interactions with caregivers, and children’s capacities for shaping and selecting their experiences increase as they mature. The temperamentally difficult child is likely to evoke more negative responses from parents; when parents themselves are under stress, or find it hard to maintain consistency, troublesome child behaviours can play a key role in fuelling harsh or punitive responses. Delinquent adolescents may seek out delinquent peers, who further encourage their antisocial activities. Associations between environmental factors and disorder often involve complex reciprocal patterns of effects.

Some of the evocative effects of children’s behaviour will reflect heritable traits.⁽²⁾ The advent of behaviour–genetic studies in child psychiatry has provided important insights into environmental as
well as genetic risks. Genetic analyses have shown, for example, that many ostensibly ‘environmental’ factors include some element of genetic mediation.⁽³⁾ Parents provide children not only with their environments but also with their genes, so that in biologically related families, nature and nurture are inevitably interwoven. Musical parents will encourage their children to enjoy music, buy them a violin, and may also pass on musical talents. In a similar way, antisocial parents may rear children in hostile and punitive environments, provide models of antisocial behaviour, and also pass on genes that predispose to disruptive behaviours. In all likelihood, genes and environments will often be correlated in this way.

Genetically informative studies have also highlighted other key mechanisms in gene-environment interplay.⁽⁴⁾ First, environments may moderate genetic influences, such that the heritability of some traits may vary systematically with qualities of the environment. Second, genetic factors may contribute to differential sensitivity to environmental risks. Research has consistently shown marked individual differences in children’s responses to all but the most severe forms of psychosocial adversity. As yet, reasons for these differences are not well understood. They may reflect variations in the severity of exposure; individual differences in resilience or coping strategies, or in environmental sources of protection; or variations in vulnerability. Genetic predispositions clearly constitute one source of such vulnerability, and several examples of gene × environment interactions have now been documented. Finally, pre-clinical studies provide clear evidence that environments can influence gene expression through epigenesis; as yet, the extent to which processes of this kind apply in humans is unknown.

Identifying environmental factors that show links with children’s adjustment is only the first step in understanding how they function to increase risk for disorder. A variety of different mechanisms has been proposed here. Some may run through the effects of stress on the biological substrate. Exposure to aggression and hostility may influence children’s cognitive processing, leading to the development of negative cognitive sets and attributional biases. In a related way, disrupted early attachments are argued to affect the psychological structures needed for later relationship formation. Adverse experiences may lead to direct increases in negative emotionality, disruptive behaviours, and impulsiveness, or to negative interactional styles that impact on social relationships. And finally, stress may affect children’s self-concepts, or compromise their coping skills in ways that increase the risks for disorder. Any given environmental risk may be associated with a number of risk mechanisms, and the processes involved in the persistence of disorder may differ from those involved in its onset.

Some vulnerability to psychopathology is laid down in foetal development. The potential for adverse effects of maternal substance use on the developing foetus have been known for many years; much recent attention has focussed on associations between prenatal cigarette smoking and risk for externalizing disorders in offspring. In addition, current estimates suggest that as much as 15 per cent of the load of childhood emotional/behavioural problems may be attributable to exposure to maternal anxiety and stress in pregnancy. Though the mechanisms involved here remain to be elucidated, there is speculation that these effects may reflect foetal programming of stress response systems akin to those posited in studies of early life influences on risk for cardiovascular disease.

Post-natally, as children progress from the complete dependence of infancy to increasing independence, they need stable and secure family relationships to provide emotional warmth, responsiveness, and constructive discipline. The influential work of Bowlby⁽⁵⁾ and others has shown that a child’s need to be attached to others is a basic part of our biological heritage. Infants become increasingly socially responsive over the first 6 months of life. At 6 to 8 months of age they begin to form selective attachments to particular individuals; they seek proximity to these attachment figures if distressed or frightened, and protest if the person they are attached to leaves. In evolutionary terms, these behaviours function to provide protection for the infant, and to reduce anxiety and distress.

Almost all infants—even those neglected or maltreated by their carers—develop attachment relationships of this kind. Their quality varies, however, depending on characteristics of the parent, the child, and the mesh between the two. Infants who have received sensitive and responsive care tend to show secure attachment patterns; insecure attachments are more likely to develop when parents themselves are stressed or unsupported, and are unresponsive to their children. Two main types of insecure attachment have been identified: avoidant attachments (associated with rejecting or highly intrusive parental care) and resistant–ambivalent patterns (associated with inconsistent or unresponsive parenting). More recently, a third disorganized category has been described, in which infants show a variety of contradictory behaviours after brief separations, and often appear confused, depressed, or apprehensive. This seems especially associated with parental behaviours that are frightening, unpredictable, or abusive.

Attachment theorists argue that the quality of these early relationships may have long-term implications. Though not entirely resistant to change, infants’ attachment patterns do tend to be stable over time. Some of this stability may reflect continuity in the quality of family care. In addition, attachment theory proposes that early attachment experiences are internalized in internal working models of self and others, which function as templates for future relationship formation. Children who have experienced responsive early care come to expect others to be caring and reliable; those who have been ignored or rejected develop less positive expectancies of others, of relationships, and of themselves. Later in development, new relationships may be created in line with these expectancies.

Although many aspects of these models await confirmation, securely attached infants are known to go on to be more sociable and co-operative in their social relationships, and to show more positive affect and self-esteem. Insecurely attached infants show less positive relationships, and are at some increased risk for psychopathology. Taken alone, attachment security in infancy is only a weak predictor of global functioning in early adulthood, suggesting that early attachment experiences work with and through other experiences—including peer relationships, later family experiences, and eventually mature intimate relationships—to contribute to later functioning. In addition, both ICD-10 and DSM-IV recognize two varieties of attachment disorders: non-attachment with emotional withdrawal, typically associated with abuse, and non-attachment with indiscriminate sociability, most usually observed when
children have been exposed to repeated changes of caretaker or institutional care. Although as many as 40 per cent of infants receive insecure attachment classifications, these more severe forms of attachment disorder are rare.