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Offender Rehabilitation: A Normative Framework for Forensic Psychologists

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Offender Rehabilitation: A Normative Framework for Forensic Psychologists

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https://www.tandfonline.com/doi/abs/10.1080/13218710802101597

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Adverse Childhood Experiences in children at high risk of harm to others. A gendered perspective.

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Adverse Childhood Experiences in children at high risk of harm to others. A gendered perspective.

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What is the prevalence of Adverse Childhood Experiences in the IVY sample?
What is the prevalence of bereavement in the IVY sample?
Are there any differences between males and females in the IVY sample?
What is the relationship between Adverse Childhood Experiences and key health and social
outcomes in the IVY sample?

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Applying the Risk Principle to Sex Offenders: Can Treatment make some sex offenders worse? 

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Applying the Risk Principle to Sex Offenders: Can Treatment make some sex offenders worse? 

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Applying-the-Risk-Principle-to-Sex-Offenders-Can-Treatment-Make-Some-Sex-Offenders-Worse.pdf (researchgate.net)

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What are the biological effects of childhood trauma ?

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What are the biological effects of childhood trauma ?

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968319/

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I. Synopsis

Trauma in childhood is a grave psychosocial, medical, and public policy problem that has serious consequences for its victims and for society. Chronic interpersonal violence in children is common worldwide. Developmental traumatology, the systemic investigation of the psychiatric and psychobiological effects of chronic overwhelming stress on the developing child, provides a framework and principles when empirically examining the neurobiological effects of pediatric trauma.

Despite the widespread prevalence of childhood trauma, less is known about trauma's biological effects in children as compared to adults with child trauma histories; and even less is known about how these pediatric mechanisms underlie trauma's short-term and long-term medical and mental health consequences. This article focuses primarily on the peer-reviewed literature on the neurobiological sequelae of childhood trauma in children and adults with histories of childhood trauma. We also review relevant studies of animal models of stress to help us better understand the psychobiological effects of trauma during development. Next, we review the neurobiology of trauma, its clinical applications and the biomarkers that may provide important tools for clinicians and researchers, both as predictors of posttraumatic stress symptoms and as useful tools to monitor treatment response. Finally, we offer suggestions for future researchers.

Keywords: Childhood trauma, developmental traumatology, developmental psychopathology, posttraumatic stress symptoms, stress, biological stress systems, brain development, genes, polymorphisms, epigenetics, cortisol

III. Introduction

Trauma in childhood has serious consequences for its victims and for society. For the purposes of this critical review, childhood trauma is defined according to the Diagnostic and Statistical Manual of Mental Disorders IV and V as exposure to actual or threatened death, serious injury, or sexual violence [ 1, 2]. This includes experiences of direct trauma exposure, witnessing trauma or learning about trauma that happened to a close friend or relative. In children, motor vehicle accidents, bullying, terrorism, exposure to war, child maltreatment (physical, sexual, and emotional abuse; neglect) and exposure to domestic and community violence are common types of childhood traumas that result in distress, posttraumatic stress disorder (PTSD), and posttraumatic stress symptoms (PTSS). Childhood traumas, particularly those that are interpersonal, intentional, and chronic are associated with greater rates of PTSD [ 3], PTSS [ 4, 5], depression [ 6] and anxiety [ 7], antisocial behaviors [ 8] and greater risk for alcohol and substance use disorders [ 9- 12].

The traditional categorical cluster of symptoms that form the diagnosis of PTSD are each associated with differences in biological stress symptoms and brain structure and function; and are thought to individually contribute to delays in or deficits of multisystem developmental achievements in behavioral, cognitive and emotional regulation in traumatized children and lead to PTSS and co-morbidity [ 13]. Thus, we examine PTSD as a dimensional diagnosis encompassing a range of pathological reactions to severe stress, rather than as a dichotomous variable.

Developmental traumatology, the systemic investigation of the psychiatric and psychobiological effects of chronic overwhelming stress on the developing child, provides the framework used in this critical review of the biological effects of pediatric trauma.[ 13] This field builds on foundations of developmental psychopathology, developmental neuroscience, and stress and trauma research. The DSM-IV-TR diagnosis of PTSD is made when criterion A, a Type A trauma, is experienced and when three clusters of categorical symptoms are present for more than one month after the traumatic event(s). These three clusters are Criterion B: intrusive reexperiencing of the trauma(s), Criterion C: persistent avoidance of stimuli associated with the trauma(s), and Criterion D: persistent symptoms of increased physiological arousal.[ 1] These criteria are complex and each Criterion is thought to be associated with dysregulation of at least one major biological stress system as well as several different brain circuits. This makes both the psychotherapeutic and the psychopharmacological treatment of individuals with early trauma complex and challenging.

Criterion symptoms have an experimental basis in classical and operant conditioning theory, where animals learn to generalized behaviors based on previous experiences or "reinforcements"[ 14] and in animal models of learned helplessness where animals under conditions of uncontrollable shock do not learn escape behaviors, and have exaggerated fear responses as well as social isolation and poor health [ 15]. For example, Cluster B reexperiencing and intrusive symptoms can best be conceptualized as a classically conditioned response that is mediated by the serotonin system and is similar in some ways to the recurrent intrusive thoughts experienced in obsessive compulsive disorder, where serotonin and norepinephrine transmitter deficits play an important role [ 16]. An external or internal conditioned stimulus (e.g., the traumatic trigger) activates unwanted and distressing recurrent and intrusive memories of the traumatic experience(s) (e.g., the unconditioned stimulus). However, other Criterion B symptoms, such as nightmares or night terrors, may involve the dysregulation of multiple neurotransmitter systems (serotonin, norepinephrine, dopamine, choline, gamma-amino butyric acid (GABA) [ 17]). Criterion C symptoms represent both avoidant behaviors and negative alterations in cognitions. In the DSM-V, Criterion C was divided into avoidant behaviors and Criterion D negative alterations in cognitions [ 2]. Avoidant behaviors can be thought of as ways to control painful and distressing reexperiencing of symptoms. These symptoms are likely associated with the dopamine system and overactivation of the opioid system and associated with anhedonia and numbing of responses [ 18]. In the DSM-IV the former Criterion D persistent symptoms of increased physiological arousal and reactivity is now Criterion E, and likely involves dysregulation of several biological stress systems [ 13, 19] as discussed in further detail below.

We will review the known differences in pediatric victims' stress biology compared to those children who have not experienced trauma. These differences are likely the causes of the greater rates of psychopathology (PTSD, depression, disruptive behaviors, suicidality, substance use disorders) and of the common medical disorders (cardiovascular disease, obesity, chronic pain syndromes, gastrointestinal disorders, immune dysregulation) seen in child victims [ 20]. Throughout, we will associate the relationship to biological stress systems and common stress symptoms. On many levels, childhood trauma can be regarded as "an environmentally induced complex developmental disorder"[ 13].

Exposure to a traumatic event or series of chronic traumatic events (e.g., child maltreatment) activates the body's biological stress response systems [ 21- 23]. Stress activation has behavioral and emotional effects that are similar to individual PTSS symptoms [ 24]. Further, an individual's biological stress response system is made up of different, interacting systems, that work together to direct the body's attention toward protecting the individual against environmental life threats and to shift metabolic resources away from homeostasis and toward a "fight or flight" (and/or freezing) reaction [ 19, 25]. The stressors associated with the traumatic event are processed by the body's sensory systems through the brain's thalamus, which then activates the amygdala, a central component of the brain's fear detection and anxiety circuits. Cortisol levels become elevated through transmission of fear signals to neurons in the prefrontal cortex, hypothalamus, and hippocampus, and activity increases in the locus coeruleus and sympathetic nervous system. Subsequent changes in, catecholamine levels contribute to changes in heart rate, metabolic rate, blood pressure, and alertness [ 19]. This process also leads to the activation of other biological stress systems.

In the review of the pertinent literature section, we will review the main biological stress response systems. We will focus on the limbic-hypothalamic-pituitary-adrenal (LHPA) axis, and the locus coeruleus-norepinephrine/sympathetic nervous system (SNS) or catecholamine system. We will also review the serotonin system, oxytocin and the oxytocin system, the immune system, and new data in genetic and epigenetic factors and gene-environment interactions that influence these systems and contribute to an individual's experience of vulnerability and resilience to childhood trauma. For each of these systems, we will provide an explanation of the mechanisms that drive them, followed by an examination of how these systems compare in children and adults who have been exposed to childhood trauma, thereby highlighting how early life adversity can disrupt the body's ability to regulate its response to stress.

Experiencing trauma during development along with dysregulation of biological stress systems can adversely impact childhood brain development [ 13] and we will discuss brain imaging studies in children who experienced trauma and adults with trauma histories. Recently, the field of neuroscience has become increasingly aware of gender as an important moderator of experience, so throughout, we review peer reviewed publications that highlight gender differences, if available. Little is known about trauma's neurobiological, genetic, and epigenetic effects in children as compared to adults with trauma histories. Since longitudinal psychobiological research in pediatric trauma is a severely understudied area, most of our review will be based on cross-sectional studies. Although we will highlight studies where longitudinal research is available, more longitudinal research in trauma-exposed children is needed to understand the pediatric mechanisms underlying trauma's short-term and long-term adverse effects in adolescence and adulthood. We will review the clinical applications of this knowledge and discuss how stress related biomarkers may provide important tools for clinicians and researchers to objectively examine predictors of PTSS and to monitor treatment response. We then offer suggestions for future directions.

A literature search of Pubmed and PsychInfo articles published to 2013 using keywords and MeSH terms "childhood," "trauma," "stress," and/or "posttraumatic stress," where crossed individually with "hypothalamic pituitary axis (HPA)", "corticotrophin releasing hormone" corticotrophin releasing factor," "immune," "serotonin," "dopamine," "oxytocin," "brain,", "brain imaging," "brain structure," "brain function," "cognitive," "genes," "polymorphisms," and "epigenetics," that were limited to the English language, were reviewed and selected for this critical review. Trauma studies involving physical head trauma or medical illnesses were not included. Our criteria were that the articles be peer-reviewed and methodologically sound, with emphasis placed on the paucity of longitudinal studies in this field. When reviews were needed to describe the foundations of biological stress systems and brain development, meta-analyses or peer-reviewed critical reviews published by known stress researchers were cited.

IV. Review of the pertinent literature: The Neurobiology of Biological Stress Systems Limbic-Hypothalamic-Pituitary-Adrenal (LHPA) Axis

The LHPA axis plays a central role in regulating the body's response to stress and is the most studied biological stress system in animals and humans. Activation of the LHPA axis triggers the hypothalamus to secrete corticotrophin releasing hormone (CRH). This neuropeptide, also called corticotrophin releasing factor (CRF), is a key mediator of the stress response [ 26]. The term CRH is used when describing its function in the neuroendocrine system and the term CRF is commonly used when describing its function as a neurotransmitter. However the term CRH is the older term and authors are not always consistent in using these rules. CRH stimulates the release of adrenocorticotrophic hormone (ACTH) by binding to CRH receptors in the anterior pituitary. ACTH in turn binds to G protein-coupled receptors in the adrenal cortex, especially in the zona fasciculata of the adrenal glands. ACTH also stimulates the secretion of cortisol, a glucocorticoid hormone that plays an important role throughout the central nervous system (CNS). Cortisol activates glucocorticoid and mineralocorticoid receptors, which are located and expressed throughout the brain. Glucocorticoid receptors act as transcription factors and regulate gene expression for metabolism and immune function, as well as for cognitive and brain development [ 27]. Increased levels of cortisol suppress the immune system, gluconeogenesis, and inhibit its own secretion via negative feedback to glucocorticoid receptors in the hippocampus [ 19].

CRF is widely distributed throughout the brain and is involved in the stress response and learning and memory [ 28]. Cortisol regulates the stress response system both in the hippocampus and medial prefrontal cortex (mPFC), where it works to attenuate the stress response, and in the medial and central nuclei of the amygdala, where it works to promote the stress response via CRF-1 receptors [ 29]. Through negative feedback, cortisol controls its own secretion, inhibiting the hypothalamus' release of CRH and the pituitary's release of ACTH, thereby bringing the body back to a state of homeostasis rather than arousal[ 19]. Cortisol levels have a consistent diurnal pattern where levels are typically close to their peak during morning awakening, rise further in the 20-minute period after awakening and then progressively fall, reaching the nadir in the afternoon in children [ 30] adolescents [ 31], and adults [ 32]. Furthermore, cortisol levels and pituitary volumes increase with age [ 33].

The LHPA Axis and Childhood Trauma

Exposure to severe stress and trauma in youth can disrupt the regulatory processes of the LHPA axis across the life span in both animals and humans [ 26, 27, 34- 36]. In animals, injections of CRF in early life produces a delayed effect in later life that is associated with reduced cognitive function, reduced number of number of CA3 hippocampal neurons, and decreased branching of hippocampal pyramidal neurons [ 37, 38]. Although the pediatric trauma literature suggest that the LHPA system is dysregulated in youth exposed to trauma, the cortisol regulation data seem contradictory, where baseline morning and 24-hour cortisol concentrations showed no differences [ 39, 40] , were higher [ 41- 47] or in a few studies, lower[ 47- 49] compared to youth without trauma. Additionally, no cortisol response differences [ 39, 50, 51], blunted cortisol responses[ 52], and increased cortisol concentration responses [ 53, 54] have been reported in maltreated children and adults with histories of childhood maltreatment under psychological and pharmacological challenges. Other measures of the LHPA axis such as ACTH also show these contradictory findings where both blunted [ 39, 55] and increased [ 50, 53, 54, 56] ACTH levels have been reported in maltreated depressed children and adults with histories of childhood maltreatment under psychological and pharmacological challenges. Furthermore, in one meta-analysis, lower morning but higher afternoon/evening cortisol levels, a flatter diurnal rhythm, and greater daily cortisol output were seen in adults retrospectively reporting trauma[ 47]; while another meta-analysis demonstrated that individuals with adulthood trauma exposure and adults with PTSD showed no differences in cortisol levels [ 57], indicating that the developing LHPA axis is vulnerable to dysregulation as a result of childhood trauma.

As outlined by De Bellis [ 13, 39, 42] , the discrepant findings described above may be related to several mediator and moderator mechanisms. A detailed examination of the factors associated with these mechanisms is important in studies endophenotyping an individual's response to the effects of early trauma on the development of biological stress systems. Endophenotyping is a term which is used to describe emotional and behavioral symptoms into stable phenotypes or observable traits with genetic associations. Identifying endophenotypes in traumatized children will be an important new tool for novel approaches to treatments such as personalized medicine [ 58]. Several of these mediation and moderation mechanisms for the biological effects of trauma on the developing child can be found in a previously published critical review (i.e., Figure 2[ 13]) and twelve updated mechanisms are detailed below for the LHPA system as this system is the most studied, providing the most data to synthesize into mechanisms (see Figure 1 ). Other biological stress systems will be reviewed and these mechanisms discussed only if there are published data available.

1. Permanent changes occur as a result of childhood trauma onset

Elevated central CRH and CRF occurs with the onset of trauma. While this CRF elevation persists into adulthood; initial elevations of ACTH and cortisol levels become attenuated with chronic exposure to elevated CRH (a.k.a. CRF). High CRH in turn causes adaptive down-regulation of pituitary CRH and neural CRF receptors after trauma onset. These ideas agree with McEwen's [ 26] theory of allostatic load, which hypothesizes that organisms adapt to re-regulate psychobiological responses to chronic stress to prevent physical harm to the organism. Increasing allostatic load over the lifespan, however, increases vulnerability to stress disorders in response to new stressors. Thus, this down-regulation of CRF receptors may be an adaptive mechanism that regulates pituitary hypertrophy (a finding seen in maltreated children with PTSD[ 59]); while a down-regulation of CRF receptors would make neurons less responsive to CRF induced neuronal damage and seizures [ 60, 61]. It should be noted that the opposite of chronic stress (i.e. environmental enrichment) delays seizures and neuronal damage in seizure prone animals through a CRF mechanism [ 62]. In support of this idea, higher levels of cerebrospinal fluid (CSF) CRF are seen in juvenile primates raised under unpredictable and adverse early rearing conditions [ 63] which longitudinally persists into young adulthood[ 64]. CSF CRF levels are higher in adults with childhood trauma histories [ 20]. In combat-related PTSD, elevated levels of central CRH were found [ 65, 66]; childhood trauma is also a risk factor for a diagnosis of PTSD after combat experiences [ 67]. Chronically elevated CRF causes generalized arousal, anxiety, aggression, hypervigiliance, and stimulation of the sympathetic nervous system (SNS), all core symptoms of the PTSD hyperarousal cluster [ 24]. It also causes inhibition of feeding and sexual behavior, core symptoms of major depression, another common outcome of traumatic experiences in childhood [ 68].

2. Childhood trauma re-regulates biological stress systems

The long-term consequence of early trauma experiences and elevated CRF resets the regulation of the LHPA axis so that ACTH and cortisol secretions are set at lower 24-hour levels during baseline and non-stressful conditions. Adult studies of victims of childhood trauma consistently show lower cortisol levels [ 47, 69]. In a meta-analysis, one of the most robust findings was that the longer the time since the trauma, the lower the morning cortisol, daily cortical volume, ACTH and postdexamethasone cortisol levels [ 47]. Since the adult PTSD studies focus on past trauma, the latter hypothesis may best explain the main differences in the data in childhood PTSD studies, where higher baseline cortisol levels were reported in most pediatric studies [ 41- 47]; while lower 24 hour cortisol levels were seen in adults maltreated in youth [ 69]. This attenuation hypothesis is supported by data from the only longitudinal psychobiological study published to date; where nonstress cortisol levels were assessed at six time points from childhood through young adulthood in sexually abused and non-abused girls. In this study, nonstress cortisol activity was initially significantly higher in sexually abused girls (post abuse disclosure) compared to non-abused girls; but cortisol activity was significantly attenuated starting in adolescence and significantly lower during young adult follow-up compared to non-abused females [ 70].

3. Priming also called sensitization occurs as a result of childhood trauma

Priming occurs as a reflection of chronic compensatory adaptation of the LHPA axis long after trauma exposure, and it may be more likely to occur after pubertal maturation. Thus, studies which show greater cortisol or ACTH response after childhood trauma exposure may be the result of "priming." LHPA axis regulation is affected by other hormones that are stress mediated such as arginine vasopressin and the catecholamines, both of which act synergistically with CRH.[ 19] A 'primed system' will 'hyper'-respond during acute stress or during the occurrence of traumatic reminders because of the interactive neuroendocrine and neurotransmitter effects activated by current life stressors on the dysregulated LHPA axis. Another term used to describe priming is sensitization, defined as enhanced neuroendocrine, autonomic and behavioral responsiveness to stress as well as LHPA axis dysregulation [ 20, 71]. Thus, when a new emotional stressor or traumatic reminder is experienced, the LHPA axis response will be enhanced (higher ACTH and higher cortisol levels). This has been seen in findings of increased ACTH secretion in depressed, abused youth who were continuing to experience chronic adversity [ 50] as well as in depressed women with a history of abuse who reported more recent chronic mild stress than abused women without major depressive disorder, who had blunted ACTH responses to CRF [ 56]. In a study of post institutionalized children that examined the effect of interactions between children and their caregivers, basal cortisol levels increased in response to parental interactions only in children who had previously been exposed to severe neglect from institutional rearing [ 72]. In addition, a prolonged elevation in cortisol levels occurred only when the previously neglected children were interacting with their caregivers, as interactions with unfamiliar adults led to similar cortisol levels in previously neglected and non-neglected children. These results therefore illustrated that previously neglected children generalized caregiver interactions as traumatic reminders and stressful experiences and thus demonstrated a disruption in the regulatory processes of the LHPA axis in response to these social interactions. Moreover, in adults with a history of child abuse, higher cortisol levels occur after exposure to traumatic reminders compared to neutral memories [ 73]. These results are the effects of 'priming' or sensitization.

4. Trauma timing and duration influence biological stress systems

Timing of trauma such as duration (single episode or chronic), age of trauma onset and stage of development influence cortisol levels post trauma. Cross-sectional studies show that trauma in infant primates [ 74] and very young or prepubertal children living in orphanages show low morning and daytime cortisol production [ 75], suggesting that prepubertal children may be more sensitive to negative feedback control mechanisms for cortisol output than older school-age children who show higher cortisol levels [ 41- 47]. Sexually abused prepubertal children with major depression exhibited significantly lower mean baseline ACTH concentrations over the first 4 hours after sleep onset compared with control children[ 76]. Results of these cross-sectional studies suggest tight down-regulation of ACTH and cortisol due to elevated central CRF in very young children. Pituitary volumes increased with age [ 59] along with increasing cortisol levels, which are also associated with increasing body fat [ 77]. Significantly larger pituitary volumes are seen in pubertal and postpubertal maltreated children and adolescents with PTSD compared with non-maltreated controls [ 59]. Thus, elevated central CRH levels may lead to pituitary hypertrophy in traumatized children, which may be most pronounced during very early childhood and puberty, due to trophic factors. An adaptive response to elevated CRH levels, particularly during the sensitive periods of very early childhood and adolescence to elevated CRH levels, must be down-regulation of CRH receptors, or the resultant high cortisol levels would result in medical illness and brain structure damage. Tight control of cortisol secretion in infancy and attenuation of cortisol secretion after trauma onset and in response to increasing levels of cortisol that occur with increasing age and puberty are in accord with the theory of allostatic load [ 26], which hypothesizes that organisms adapt to chronic stress to prevent physical harm.

5. Individual differences in response to childhood trauma are associated with different types of biological stress system regulation

Individual differences in behavioral and emotional responses are associated with different types of LHPA axis dysregulation. Most studies show LHPA axis dysregulation consistent with elevated central CRF in youth who experience childhood trauma and depressive and anxiety symptoms [ 39, 41- 47, 50, 78- 80] or co-morbid internalizing and internalizing behaviors [ 42, 79]; while traumatized children with marked disruptive behavioral disorders or anti-social behaviors show lower cortisol levels [ 81].In addition, in a study of adults with moderate to severe child maltreatment histories and no diagnosable psychopathology, lower concentrations of cortisol and ACTH were seen in response to the Trier Social Stress Test compared to healthy adults without maltreatment histories [ 82], further suggesting that elevated central CRF is likely seen as a result of maltreatment even in resilient outcomes.

6. Early trauma type and trauma severity influence biological stress systems

Certain trauma types and increased overall trauma severity are more likely to result in LHPA dysregulation. For example, children who suffered from physical and sexual abuse occurring in the first 5 years of life were more likely to experience internalizing symptoms and LHPA axis dysregulation than those who suffered from abuse occurring after age 5, or from neglect, or emotional abuse [ 40]. Increasing severity of childhood trauma is associated with dysregulation of the LHPA axis. Children who experienced multiple maltreatment or those who experienced severe sexual abuse were more likely to have elevated cortisol levels [ 44]. Furthermore, in maltreated children with PTSD, 24 hour urinary cortisol concentrations correlated positively with increased trauma duration, and with PTSD intrusive and hyperarousal symptoms [ 42].

7. Genetic factors influence biological stress system responses to childhood trauma

LHPA-related genetic factors influence the effect of childhood trauma on the LHPA axis and its associated outcomes. Gene × environment interplay is important for the expression of both negative and resilience outcomes following childhood trauma. Gene x environment investigations are a relatively new area of study, so these data should be considered preliminary since this part of the field is still in its infancy.

Polymorphisms are normal variations in genes, which code for important proteins that build the body and its functions. Single nucleotide polymorphisms (SNPs) are the most common type of genetic variation. Specific polymorphisms that are needed to form LHPA axis related structures (CRH and glucocorticoid receptors) appear to moderate the effect of child abuse on the risk for childhood neuroticism and adult depressive symptoms. The brain's CRH type 1 receptors (CRHR1) are located throughout the brain [ 27] and, when activated, produce symptoms of anxiety and depression [ 24, 83].

There are few studies of gene × environment interplay in children. In one study, physically abused, emotionally abused, and neglected children who carried two copies of the TAT haplotype of the CRHR1 had significantly higher levels of neuroticism, a prelude to anxiety and depression, than non-maltreated children who had two copies of the TAT haplotype [ 84]. However, in this study, sexually abused children and children who had experienced 3 or 4 types of abuse, who had two copies of the TAT haplotype appeared to be protected from neuroticism compared to children who experienced other types of maltreatment [ 84]. In a follow-up study of these children, only maltreated children who carried two copies of the TAT haplotype exhibited a blunted slope of diurnal cortisol change, a sign of increasing allostatic load and dysregulation of the LHPA axis. However, the CRHR1 haplotype groups (zero or one copy vs. two copies) were not related to internalizing symptoms [ 85].

In contrast, one study of adult carriers of both the TCA (i.e., T-alleles, formed of SNP, rs7209436, and C allele formed by SNP rs4792887) and TAT haplotypes (i.e., A-allele formed of SNP rs110402) as well as the 2 SNPs (rs7209436 and rs242924) located in intron 1 of the CRHR1 gene, were significantly protected from having major depression despite histories of child abuse [ 86]. This finding was replicated in a relatively large study of women with child maltreatment [ 87], and in African American men and women [ 88], but not replicated in a study of European men and women, who experienced childhood maltreatment [ 87]. On the other hand, adults with moderate to severe child maltreatment histories and the GG polymorphisms of the CRHR1 gene (rs110402) showed a significant interaction with maltreatment for increased cortisol responses to dexamethasone/corticotropin-releasing hormone pharmacological challenge compared to those adults with maltreatment and the A allele [ 88]. Higher cortisol is a well-replicated finding in adults with major depression [ 19, 89]. Furthermore, sex effects may be important in gene × environment interplay. In another study of adults with child abuse histories, the protective effect of the CRHR1 polymorphisms (rs110402 A-allele) against developing adult depression and with decreased cortisol response in the dexamethasone/ corticotropin-releasing hormone pharmacological challenge were observed only in men, and not in women [ 90] , a finding opposite to the one described above [ 87].

Gene × environment interplay was seen in a prospective study of the FKBP5 gene, a gene that inhibits glucocorticoid-receptor-mediated glucocorticoid activity [ 91]. In this study, 884 Caucasians with no history of depression were enrolled at age 12 to 14 years, and followed for 10 years [ 92]. Those who were homozygous for the minor alleles and had traumatic (but not separation (i.e., lost of parent through death or divorce) events (particularly severe child maltreatment) prior to age 24 years, showed an increased incidence of depression on follow-up, suggesting that the minor allele of the FKBP5 polymorphism and childhood trauma interacted to predict adult depression. Three variants in the FKBP5 gene (rs4713916, rs1360780, and rs3800373) were associated with a failure of cortisol responses to return to baseline in healthy adults after psychosocial stress, suggesting a genotype-dependent risk of chronically elevated plasma cortisol levels in the context of acute stress as a possible mechanism for the increased risk of stress related mental disorders, such as depression and PTSD in adults with these alleles [ 93]. Cross-sectional studies have also found interaction for adults who carry the minor FKBP5 allele and have child maltreatment histories as they have increased rates of depression [ 94], PTSD [ 95, 96], and suicide risk [ 97]. Interestingly, in one cross sectional study, the less common FKBP5 haplotype (H2) was associated with an increased risk of overt aggressive behavior in adult male prisoners who have a history of physical abuse[ 98]. In an imaging study, healthy young adults, were genotyped for 6 FKBP5 polymorphisms (rs7748266, rs1360780, rs9296158, rs3800373, rs9470080 and rs9394309) previously associated with psychopathology and/or LHPA axis function [ 99]. Interactions between each SNP and increased levels of emotional neglect, were associated with heightened reactivity to angry and fear faces in the dorsal amygdala which suggests a neurobiological mechanism linking PTSS and depressives symptoms of hyperarousal and hypervigilience to negative affect and to psychopathology [ 99]. Hence, investigations of gene × environment interplay suggest that risk genes may interact with childhood trauma to produce different adult emotional, behavioral, and neurobiological outcomes.

8. Epigenetic factors influence biological stress system responses to childhood trauma

LHPA-related epigenetic factors influence the effect of childhood trauma on the LHPA axis and its associated negative behavioral and emotional outcomes. Epigenetics is also a relatively new area of study, so the limited data to date will be described here. The epigenome consists of chromatin, the protein-based structure around DNA, and a covalent modification of the DNA itself by the methylation of cytosine rings found at CG dinucleotides [ 100]. The epigenome determines the accessibility of the DNA to convert genetic information into the messenger RNA necessary for gene function. Early traumatic experiences are associated with hyper- and demethylation of specific regulatory sites in key biological stress system genes including the gene encoding of the glucocorticoid receptor [ 101] and the neuropeptide arginine vasopressin (AVP) which is co-localized with CRH and released with CRH from the paraventricular nucleus of the hypothalamus during stress [ 102]. Increased methylation of key biological stress system genes can silence a gene's activity by making the gene inaccessible for transcription, while demethylation may make a gene accessible for transcription. Thus, childhood trauma can have a long-term impact on gene activity without changing an individual's DNA sequence (i.e., genes)[ 103, 104]. Epigenetic effects may account for the inconsistent main gene and gene x environment results in the studies previously reported.

Animal studies have provided the first evidence of epigenetic effects caused by early trauma. Rats developing in optimal environments show less stress reactivity [ 105]. Because lactating female Long-Evans rats exhibit individual variation in the frequency of pup licking/grooming, high or low levels of pup licking/grooming are considered a maternal phenotype [ 106]. As adults, the offspring of high licking/grooming mothers show less plasma ACTH and cortisol responses to acute stress in comparison with animals reared by low licking/grooming mothers [ 106, 107]. The offspring of high licking/grooming mothers also show significantly increased hippocampal glucocorticoid receptor mRNA and protein expression, enhanced glucocorticoid negative feedback sensitivity, and decreased hypothalamic CRF mRNA levels, which all indicate decreased stress reactivity as a result of optimal quality of care.[ 105] Furthermore, DNA methylation patterns differ in high licking/grooming versus low licking/grooming offspring. The glucocorticoid receptor promoter sequence in the hippocampus of adult offspring of low licking/grooming mothers is hypermethylated and functionally less sensitive to cortisol feedback. Maternal behaviors also affect other biological systems that are associated with the LHPA axis. Prolonged periods of maternal separation alter the methylation state of the promoter for the arginine vasopressin gene (AVP) in the pup, increasing hypothalamic vasopressin AVP synthesis and LHPA responses to stress, along with memory deficits and learned helplessness behaviors [ 108].

In a rodent model of infant maltreatment, abuse and neglect during infancy decreases brain-derived neurotropic factor (BDNF) gene expression in the adult prefrontal cortex (PFC) [ 109]. In addition, these investigators found that chronic treatment with a DNA methylation inhibitor lowered levels of methylation in male and female rats exposed to early maltreatment. They also showed not only that infant trauma was associated with poor mothering in the next generation and that these epigenetic changes in DNA methylation were passed on from one generation to the next generation, even if the offspring of an abusive dam (mother rat) was cross-fostered with a non-maltreating dam, thereby indicating heritability of these epigenetic changes [ 109].

Increased methylation in a neuron-specific glucocorticoid receptor (NR3C1) promoter was seen in human postmortem hippocampus obtained from suicide victims with a history of childhood abuse compared to suicide victims without child abuse histories and controls who died of non-suicide related causes, demonstrating an association between early trauma and epigenetic alterations [ 101]. Decreased hippocampal glucocorticoid receptor expression due to epigenetic changes likely increased LHPA activity and enhanced the risk of both depression and suicide in adults who were child abuse victims [ 101]. These findings link the previously described data from rats to humans and suggest a common effect of quality of parental care on the epigenetic regulation of hippocampal glucocorticoid receptor expression that can lead to health or the LPHA axis dysregulation seen in childhood PTSD and PTSS and adult depression.

In addition, a preliminary investigation showed that experiencing foster care during childhood is associated with changes in methylation of genes related to both the HPA axis and the immune system [ 110]. This study therefore supports the idea that childhood trauma may be linked to changes in genetic expression and resulting mental and medical health problems.

9. Gender differences influence the effects of childhood trauma on biological stress systems

Gender differences influence the effect of childhood trauma on the HPA axis. Research involving men and women who were exposed to early trauma but who did not have any psychopathological diagnoses has shown stronger associations between trauma and increased CRF levels in men than in women [ 111]. In children, girls with histories of physical abuse had higher levels of urinary oxytocin, a neuroendocrine peptide that down-regulates cortisol and is associated with complex social behaviors, and lower levels of salivary cortisol following an experimental stressor when compared to non-abused girls; while abused and non-abused boys did not differ in their hormonal responses [ 112]. Early trauma and gender differences are an area of research that warrants further investigations, as a prospective investigation showed that maltreated males may be more likely to be arrested for violent offenses as adults [ 113], thus becoming prisoners and less likely to be involved in retrospective research studies. This fact can lead to a selection bias in retrospective studies, and a possibly mistaken idea that females are more vulnerable to early trauma. Early trauma experiences may lead to greater down-regulation of cortisol due to high levels of CRF and other stress markers, in males compared to females, findings that are commonly seen in individuals with antisocial behaviors [ 81].

10. Social support buffers biological stress system dysregulation and its associated negative behavioral and emotional outcomes

As adults, the offspring of high licking/grooming mothers show decreased stress and cortisol reactivity as a result of optimal quality of care [ 105]. In preschool children, quality of childcare is associated with a buffering of hypothalamic-pituitary-adrenal axis to stress [ 114]. In adult studies, social support was associated with a decrease in the cortisol response to the Trier Social Stress Test in men [ 115]. Furthermore, decreased cortisol response and activity in the dorsal anterior cingulate, a brain region involved in distress separation, were seen in response to an exclusion neuroimaging task when daily social support was part of the research paradigm [ 116]. Further research is needed on the impact of social support in traumatized children.

11. Individual biological stress systems dysregulation in response to childhood trauma and the genes associated with the function of these systems influence other biological systems during development to contribute to psychopathology

For example, the LHPA modulates the locus coeruleus-norepinephrine/SNS system and the immune system [ 19]. When the hypothalamus releases CRH in response to stress, the locus coeruleus becomes activated indirectly through the central amygdala [ 19]. Serotonin modulates LHPA activity [ 117]. Furthermore, having more than one type of a depression risk allele in two different biological stress systems (i.e., the risk CRHR1 polymorphisms in the LHPA axis and the short allele of serotonin transporter gene promoter polymorphism (5-HTTLPR) in the serotonin system) is associated with current depressive symptoms in adults with less severe levels of child abuse and neglect as measured on the Childhood Trauma Questionnaire [ 118].

12. Biological stress systems dysregulation in response to childhood trauma adversely influences cellular, cognitive and brain development [42, 119, 120]

Human brain maturation is marked by the acquisition of progressive skills in physical, behavioral, cognitive, and emotional domains. Myelin, a fatty white substance produced by glial cells, is a vital component of the brain. Myelin encases the axons of neurons, forming an insulator, the myelin sheath and is responsible for the color of white matter. Myelination of newly formed neuronal networks increases neural connectivity and parallels these developmental changes. Brain development occurs with an overproduction of neurons in utero, increases in neuron size, synapses, and neural connections during childhood and adolescence, selective elimination of some neurons (apoptosis) with corresponding decreases in some connections and strengthening of others and corresponding increases in myelination to hasten these connections. Synapses, dendrites, cell bodies, and unmyelinated axons, which form the brain's gray matter, decrease during development [ 121]. Glucocorticoids are important for normal brain maturation including initiation of terminal maturation, remodeling axons and dendrites and affecting cell survival [ 26, 122]. Both suppressed and elevated glucocorticoid levels can impair brain development and function [ 26, 122]. During brain maturation, stress and elevated levels of stress hormones and neurotransmitters may lead to adverse brain development through apoptosis [ 123- 125], delays in myelination[ 126], abnormalities in developmentally appropriate pruning [ 127, 128], the inhibition of neurogenesis[ 129- 131], or stress induced decreases in brain growth factors[ 132]. Indeed, maternal deprivation increases the death of infant rat brain cells [ 133]. Consequently, dysregulation of a maltreated child's major stress systems likely contributes to adverse brain development and leads to psychopathology [ 13].

Telomeres are the repetitive TTAGGG sequence at the end of linear chromosomes and with each division, telomeres get shorter, and are considered a molecular clock for cellular aging [ 134]. In a cross sectional study of children who were previously institutionized, telomere length was shorter than children without such histories[ 135]. In a prospective longitudinal study of children, from ages 5 to 10 years, children who experienced two or more types of violence (measured as bullying, witnessing domestic violence, and physical abuse), have increased telomere erosion, a marker of premature cellular aging, compared to children who did not experience violence [ 120]. This landmark study suggests that children, who experience trauma, have decreased telomere maintenance, a potential mechanism ("premature aging") for adverse brain development, mental health problems, and chronic health problems in adults with a childhood history of trauma [ 13, 136].

The Locus Coeruleus-Norepinephrine/Sympathetic Nervous System (SNS)/Catecholamine System and Childhood Trauma

Sexually abused girls with dysthymia demonstrated greater 24-hour levels of total urinary catecholamines than non-abused girls [ 140]. Maltreated boys and girls with PTSD showed greater levels of urinary catecholamines at baseline than non-maltreated healthy children and non-maltreated children with generalized anxiety disorder [ 42]. Urinary catecholamines positively correlated with duration of PTSD trauma and number of PTSD internalizing and child dissociative symptoms [ 42]. In a study of children who experienced motor vehicle accidents, significantly elevated plasma noradrenaline concentrations were seen prospectively, at both months 1 and 6, after the accident, compared to the non-PTSD and control groups, further suggesting that higher catecholamines occur as a result of trauma and PTSD [ 141]. In a study of police academy recruits, those with early trauma exposure demonstrated heightened 3-methoxy-4-hydroxy-phenylglycol (MHPG) (the major metabolite of norepinephrine) response after watching critical incident videos [ 142]. An adult positron emission tomography imaging study demonstrated significantly reduced norepinephrine transporter (NET) availability in the locus coeruleus in PTSD which would lead to chronic stimulation of the locus coeruleus as a result of increased levels of norepinephrine. This finding positively correlated with PTSD hypervigilance symptoms. Furthermore, in a gene x environment analysis, adult carriers of the Val allele of the Catechol-O-methyltransferase (COMT) polymorphism (a gene involved in dopamine degradation) with a history of sexual abuse showed a higher disposition toward anger, symptoms commonly seen in PTSD patients, compared with adults homozygous for the Met allele. The Val allele is associated with increased dopamine neurotransmission in the prefrontal cortex, which is associated with deficits in executive function [ 138, 139] and increased risk for impulsive anger. On the other hand, adults with early trauma and the Val/Val genotype showed increasing levels of dissociation corresponding to increased exposure to higher levels of childhood trauma [ 143]. Dissociation is a failure to integrate sense of self with current and past memories and emotions and is a pathological defense to ward off anxiety that is also associated with non-intentional antisocial behaviors. Dissociation is a different construct from depression and anxiety. Thus studies in both children and adults have consistently demonstrated higher locus coeruleus (LC)-norepinephrine/SNS system activity associated with childhood trauma and PTSD, while down-regulation of this system due to trauma may be associated with antisocial behavior and dissociation.

The Serotonin System and Childhood Trauma

Serotonin is a critical element of the stress response system [ 13]. Serotonergic neurons project diffusely from the central serotonin raphe nuclei in midbrain to important cortical and subcortical brain regions (e.g., prefrontal cortex, amygdala, hippocampus) that play known roles in regulating emotions (e.g., mood), behaviors (e.g., aggression, impulsivity)[ 144, 145], cognitive function, motor function, appetite, and the regulation of many physiological processes (e.g. cardiovascular, circadian, neuroendocrine respiratory, and sleep functions [ 144, 146]). Serotonin is an important regulator of morphogenetic activities during early brain development, influencing cell proliferation, migration, and differentiation, thus influencing child brain development [ 147]. In preclinical animal studies, decreased levels of serotonin activity are associated with increased levels of aggressive behaviors in rodents and primates exposed to early adversity [ 148]. Mice genetically engineered to lack the serotonin transport gene show increased LHPA axis activation to stress, suggesting that serotonin modulates LHPA activity [ 117]. Disruptions in serotonin's regulatory functioning are linked with several psychopathological disorders that are commonly seen in children and adults with childhood trauma. For example, decreased levels of serotonin activity have been associated with mental health problems such as depression and anxiety [ 149] as well as with aggressive behaviors in individuals with personality disorders such as borderline personality disorder[ 150].

Early trauma dysregulates serotonin in humans. The serotonin transporter protein is involved in the reuptake of serotonin from the synapse, and is critical to serotonin regulation in the brain. The short allele of the serotonin transporter gene promoter polymorphism (5-HTTLPR) interacts with maltreatment in the development of childhood depression. The short allele is associated with reduced transcriptional activity of serotonin, so that there is less central serotonin available in the brain; while the long allele has at least twice the basal level of transcriptional activity of the short variant [ 151]. Most studies regarding the effects of 5-HTTLPR are in adults maltreated as children. A large epidemiological study demonstrated that there were no main genetic effects, but carriers of the S-allele had a higher risk of developing depressive and suicidal symptoms when exposed to stressful life events and childhood maltreatment [ 152]. Children who were homozygous for the short allele of 5-HTTPR demonstrated a significantly elevated vulnerability to depression, but only in the presence of maltreatment; but the presence of positive supports reduced this risk [ 153]. Having two short-short alleles of the 5-HTTLPR gene moderated the association between bully victimization and emotional problems, such that frequently bullied children were at an increased risk as adolescents for depression or anxiety; the short-long and long-long genotypes did not confer an increased risk [ 154]. However other studies have not shown an increased vulnerability to depression as a function of interactions between the short allele and maltreatment. Instead, they have shown increased risk with the long-long allele [ 85, 155]. One study of 595 youth suggests that genetic variation has a negligible effect on promoting resilience among maltreated children [ 156]. In other words, non-maltreated children with the short-short genotype were more likely to have higher resilient functioning; while maltreated children with the short-short genotype were more likely to have lower resilience [ 156]. This study agrees with controversial meta-analyses that have found that adverse childhood events had a main effect on depressive outcomes regardless of 5-HTTLPR polymorphisms [ 157, 158]. The discrepant findings in adults may be caused by failure to include trauma versus a stressful life event, trauma age of onset, trauma duration, and trauma type in the gene x environment interaction analyses, as this interaction showing that adults with histories of child maltreatment were found in another meta-analysis to be at increased risk for depression [ 159]. On the other hand, in a forensic sample of 237 men with elevated levels of child abuse and neglect given the Childhood Trauma Questionnaire, measures of psychopathy were highest among carriers of the 5-HTTPR long allele and carriers of the low activity monoamine oxidase A (MAOA) gene [ 160]. Thus resilience is a complex issue, as psychopathy as an outcome may be more harmful to society than depressive symptoms.

Furthermore, genetic polymorphisms can have additive genetic effects. Children who were homozygous for the short allele of 5-HTTLPR, and had the val66met variant of the brain-derived neurotropic factor (BDNF) gene, and had been maltreated, were at increased risk of depression.

In summary, the serotonin system and the genes regulating the serotonin system are influenced by early trauma. However, the field has not yet advanced to the point where treatment can be tailored to an individual child. More work needs to be done on gene-gene interactions, possible epigenetic effects, trauma variables, and other factors such as social supports, to achieve this aim.

The Oxytocin System and Childhood Trauma

Oxytocin plays an important role in interpersonal relationships. Involved in the regulation of an individual's sexual response and milk production, this hormone is also responsible for the regulation of a wider range of social interactions, including social memory and cognition, emotion recognition, empathy, and attachment [ 166]. In addition, the oxytocin system is involved in the regulation of the body's response to stress. Research in rats demonstrated a relationship between oxytocin and the mother's relationship with her offspring, as those mothers who engaged in more licking/grooming behaviors exhibited higher levels of oxytocin receptor binding in the amygdala [ 167]. Similarly, rat mothers who demonstrated high levels of licking/grooming had increased levels of oxytocin gene expression and a subsequent increase in dopamine reward production. Mothers who demonstrated lower levels of licking/grooming behaviors, had lower levels of oxytocin gene expression, thereby highlighting the important role that oxytocin plays in the attachment bond [ 168].

Research involving humans has similarly demonstrated that negative life events can disrupt the body's regulation of oxytocin. Decreased levels of oxytocin have been found in women exposed to early maltreatment-a relationship that was shown to be especially strong when the form of maltreatment was emotional abuse [ 20]. Gender differences have also been found in the relationship between childhood trauma and oxytocin regulation. Focusing on oxytocin response to an experimental stressor in abused girls and abused boys, girls exposed to physical abuse exhibited higher levels of oxytocin, as well as decreased levels of cortisol, in response to the experimental stress; while there was no difference in hormone response to the stress in the abused boys [ 112]. In the Adverse Childhood Experiences Study, a relationship was found between exposure to early trauma and increased promiscuity[ 136]. To explain this relationship, the researchers pointed out that disruptions in oxytocin regulation of social attachments during childhood can lead to high oxytocin and thus problems forming fast and less discriminate personal attachments during adulthood [ 136].

On the other hand, a strong moderating effect of a positive social environment has also been found in adults with a specific allele of the oxytocin receptor gene OXTR who had been exposed to early stress, as increased resilience in adulthood was found only in those individuals who had been surrounded by a positive family environment during childhood [ 169]. Further research is needed on the impact of oxytocin on emotional and behavioral outcomes in traumatized children.

The Immune System and Childhood Trauma

Activation of the immune system involves the production of cytokines, which promote an inflammatory reaction to infection or pathogens in the body. Although one of the main effects of this reaction is to produce the physical symptoms of sickness (e.g., fever, nausea, and fatigue), activation of cytokines that promote inflammation are implicated in depression, a common outcome of early trauma [ 170]. A recent systematic review provided evidence that supports the relationship between pro-inflammatory cytokines and increased levels of depression and anxiety in adolescents [ 171]. Higher levels of plasma antinuclear antibody titers have been found in girls who have been sexually abused, suggesting that exposure to this form of stress may inhibit the body's means of suppressing the B lymphocytes, or the lymphocytes that produce antibodies, thereby leading to the increased levels of the antibody titers found in the abused girls [ 172]. Increased levels of inflammatory cytokines, as well as decreased levels of anti-inflammatory cytokines, have been associated with adult PTSD and exposure to chronic stress [ 173, 174]. In women who had experienced early maltreatment, those who had been diagnosed with PTSD had higher activation levels of T cells than those who did not have PTSD More specifically, investigators found a positive correlation between T-cell activation levels and intrusive symptoms of PTSD [ 175]. Similar results were found in a study of women with PTSD secondary to physical or sexual abuse during childhood, where these women demonstrated increased inflammatory and immune activity[ 176]. Other investigators demonstrated that greater concentrations of interleukin-6 (IL-6), a proinflammatory cytokine, concentrations were seen during the Trier Social Stress Test in adults with child maltreatment histories compared to adults without such histories [ 177]. Furthermore in a longitudinal study of a New Zealand birth cohort (n=1037), it was demonstrated that adults with histories of poverty, social isolation or maltreatment had elevated rates of depression and age-related metabolic disease risks in adulthood including higher body mass index, total cholesterol, glycalated hemoglobin, and low levels of high-density lipoprotein, low maximum oxygen consumption, and higher levels of C-reactive protein, a measure of inflammation [ 178]. Further children exposed to a greater number of these adverse childhood risk factors had greater age-related disease risk in adult life [ 178]. The increased activation of cytokines and dysregulation of the immune system, along with the other biological stress response systems, such as the HPA axis and the LC/SNS systems, that occurs in response to early adversity, can lead to hypertension, accelerated atherosclerosis, metabolic syndrome, impaired growth, and immune system suppression and poorer medical health in adults with child trauma histories [ 179].

The Effect of Childhood Trauma on Neuropsychological Functioning and Cognitive Development

In a study comparing the performance of abused youth with PTSD, abused youth without PTSD, and non-maltreated youth on comprehensive neuropsychological testing, both groups of maltreated youth performed worse than the control youth, with deficits in IQ, academic achievement, and all neurocognitive domains expect for fine-motor functioning[ 193]. The maltreated youth with PTSD showed greater deficits in visuospatial abilities than the maltreated youth without PTSD, and sexual abuse was found to be negatively associated with language and memory scores. A negative relationship was found between the number of maltreatment types experienced and academic achievement, demonstrating that cumulative trauma leads to neuropsychological problems that are unrelated to PTSD symptoms[ 193]. Data from the National Survey of Child and Adolescent Well-Being (NSCAW) study demonstrated that maltreated children who experienced maltreatment during multiple developmental periods had more externalizing and internalizing problems and lower IQ scores than children maltreated in only one developmental period suggesting that trauma duration has negative and cumulative cognitive effects [ 194].

Longitudinal prospective studies involving adolescents and adults exposed to maltreatment in childhood agree with the cross-sectional studies and have demonstrated lower IQ scores and deficits in reading ability [ 195- 200]. The research on the effects of early trauma on cognitive function indicates that early trauma is associated with adverse cognitive development and that this is likely reflected in adverse brain development.

The Effect of Childhood Trauma on Brain Development

An early, unexpected, trauma, maternal deprivation, increases the death of both neurons and glia cells in cerebral and cerebellar cortexes in infant rats [ 133]. Increased exposure to cumulative life stress (e.g., exposure to severe marital conflict, severe chronic illness of a close family member or friend) was associated with poorer spatial working memory performance and decreased volumes of white and gray matter in the prefrontal cortex of non-maltreated youth [ 201]. Pediatric imaging studies demonstrated that both cerebral and cerebellar volumes are smaller in abused and neglected youth compared to non-maltreated youth [ 202- 206]. In one research study, maltreated subjects with PTSD had 7.0 % smaller intracranial and 8.0% smaller cerebral volumes than non-maltreated children [ 119]. The total midsagital area of corpus callosum, the major interconnection between the two hemispheres that facilitates intercortical communication, was smaller in maltreated children [ 119]. Smaller cerebral volumes were significantly associated with earlier onset of PTSD trauma and negatively associated with duration of abuse [ 119]. PTSD symptoms of intrusive thoughts, avoidance, hyperarousal and dissociation correlated negatively with intracranial volume and total corpus callosum measures [ 119]. another study showed smaller brain and cerebral volumes and attenuation of frontal lobe asymmetry in children with maltreatment-related PTSD or subthreshold PTSD compared with archival non-maltreated controls [ 203].

However, these two previously described studies did not control for low socioeconomic status, which influences brain maturation through ecological variables [ 119, 207]. In another study which controlled for socioeconomic status, children with maltreatment-related PTSD had smaller intracranial, cerebral and prefrontal cortex, prefrontal cortical white matter, and right temporal lobe volumes and areas of the corpus callosum and its subregions and larger frontal lobe CSF volumes than controls [ 205]. The total midsagittal area of corpus callosum and middle and posterior regions remained smaller; while right, left, and total lateral ventricles and frontal lobe CSF were proportionally larger than controls, after adjustment for cerebral volume [ 205]. Brain volumes also positively correlated with age of onset of PTSD trauma and negatively correlated with duration of abuse [ 205]. The larger lateral ventricles were only seen in maltreated males, suggesting that males are more vulnerable to the neurotoxic effects of childhood maltreatment. Smaller cerebellar volumes were seen in male and female maltreated children with PTSD [ 204]. Younger age of onset and longer trauma duration were significantly correlated with smaller cerebellum volumes [ 204]. Smaller cerebellum volumes were also seen in previously institutionized youth [ 202]. The cerebellum is a complex posterior brain structure that is involved in cognitive functions [ 208], decision making, reward circuits [ 209, 210] and the default mode network that is associated with understanding social intentions [ 211]. Child maltreatment is also associated with adverse effects in individual brain structures that are involved in reward and default network processing. In a large study of 61 medically healthy youth (31 males and 30 females) with chronic PTSD secondary to abuse, who had similar trauma and mental health histories, and 122 healthy non-maltreated controls (62 males and 60 females), the midsagital area of the corpus callosum subregion 7 (splenium) was smaller in both boys and girls with maltreatment-related PTSD compared to their gender-matched comparison subjects [ 212]. Youth with PTSD did not show the normal age-related increases in the area of the total corpus callosum and its region 7 (splenium) compared to non-maltreated children [ 212]. This was an important finding for several reasons. The maltreated and control children were not prenatally exposed to substances and had no pregnancy or birth trauma, were psychotropically naïve, and had no history of substance abuse or dependence, thus excluding confounds which are commonly seen in maltreated children [ 213, 214] and not addressed in exclusion criteria in most neurobiological studies published to date. The axons in the splenium of the corpus callosum myelinate during adolescence and are important to the posterior reward circuits and the posterior default networks [ 215]. Additionally, clinical symptoms of PTSD intrusive, avoidant, and hyperarousal symptoms, symptoms of childhood dissociation, and child behavioral checklist internalizing T score significantly and negatively correlated with corpus callosum measures [ 212]. Children with maltreatment-related PTSD had reduced fractional anisotropy values on diffusion tensor imaging brain scans of white matter, indicating less myelin integrity in the medial and posterior corpus, a region which contains interhemispheric projections from brain structures involved in circuits that mediate emotional and memory processing, core disturbances associated with trauma history [ 216]. Smaller corpus callosum area measures were seen in another anatomical magnetic resonance imaging brain study of neglected children with psychiatric disorders compared to nonmaltreated children with psychiatric disorders, suggesting that smaller corpus callosum measures may be a consequence of maltreatment [ 217].

Another important contributor to memory and the default mode network is the hippocampus. Unlike findings in adult PTSD, where several studies reported hippocampal atrophy [ 223], maltreated children and adolescents with PTSD or subthreshold PTSD showed no anatomical differences in limbic (hippocampal or amygdala) structures cross-sectionally [ 119, 203, 205] or longitudinally [ 224]. However, investigators have demonstrated functional brain differences in the amygdala and hippocampus of maltreated youth compared to non-maltreated children [ 222, 225]. One study suggests that hippocampal atrophy may be a latent developmental effect of childhood maltreatment [ 226].

Functional neuroimaging studies of adults with PTSD related to childhood maltreatment have shown decreased levels of executive and attentional function as reflected by decreased activation in the dorsal control networks with corresponding increased activation of the amygdala and hippocampus and other structures of the affective emotional networks during emotional challenge tasks; suggesting dorsal control network deficits in adult PTSD secondary to childhood trauma [ 229- 231]. Research using functional neuroimaging of children and adolescents exposed to maltreatment has shown similar executive, attentional, and affective emotional dysregulation [ 221, 222, 232- 234]. Further, previously institutionalized children demonstrated decreased prefrontal white matter microstructural organization on measures of diffusion tensor imaging that was associated with neurocognitive deficits in spatial planning and a visual learning and memory task compared to non-neglected controls [ 235].

In another study of healthy adult women with a history of childhood sexual abuse, investigators found higher T2 relaxation time (an indirect index of resting blood volume) in the cerebellar vermis than in non-maltreated women, which correlated strongly with Limbic System Checklist ratings of temporal lobe epilepsy and their frequency of substance use [ 236]. In studies of carefully characterized healthy adults who only experienced corporal punishment without other forms of maltreatment, T2 relaxation times were increased in dopamine-rich brain decision making and reward regions (caudate and putamen, dorsolateral prefrontal cortex, substantia nigra, thalamus and accumbens)[ 237]. In the latter study, regional T2 relaxation times were significantly associated with increased use of drugs and alcohol. These studies provide further evidence that specific types of abuse and neglect contribute to the intergenerational cycle of emotional and behavioral problems as well as addiction by their detrimental impact on the brain.

Genetic factors interact with childhood trauma to influence brain structure and function. For example, adults with the Val66MET polymorphism of brain-derived neurotrophic factor (BDNF) who had a history of child maltreatment had a greater likelihood of depressive disorders and a smaller hippocampus, highlighting a child trauma x polymorphism interaction for hippocampal volume reductions [ 238]. Epigenetic factors also play a role in brain function. In a genome-wide study of promoter methylation in individuals with severe abuse during childhood trauma, decreased promoter transcriptional activity associated with decreased hippocampal expression of the Alsin variants were seen [ 239]. Adults who were maltreated as children and committed suicide showed similar hypermethylation in the nerve growth factor-induced protein A binding site within a glucocorticoid receptor variant that was associated with decreased glucocorticoid receptor expression in the hippocampus [ 101]. Mice without the expression of the Alsin gene exhibited more anxiety compared to wild type mice [ 240].

Furthermore, there are gender x maltreatment effects on brain development. Gender differences were demonstrated using anatomical MRI. Maltreated boys with PTSD had smaller cerebral volumes and larger lateral ventricular volumes than maltreated girls with PTSD, even though the two groups had similar trauma, mental health histories, and IQ [ 212]. In addition, research has shown a relationship between the type of trauma and gender, as neglect has been shown to have a strong association with smaller corpus callosum size in boys, while sexual abuse was strongly linked to decreased corpus callosum size in girls [ 217]. In a functional MRI study comparing maltreated youth with PTSD symptoms to non-maltreated youth during performance on an emotional oddball task, left precuneus/posterior middle cingulate hypoactivation to fear versus calm or scrambled face targets were seen in maltreated versus control males and may represent dysfunction and less resilience in attentional networks in maltreated males[ 241]. These findings were not seen in maltreated females with PTSD symptoms and gender by maltreatment effects were not attributable to demographic, clinical, or maltreatment parameters, suggesting that maltreated males may be dedicating significant functional neural resources to processing affective stimuli in lieu of cognitive processes, which may lead to impulsive decision-making during states of fear emotion and thus less resilience in maltreated males [ 241].

Thus, the data to date strongly suggests that childhood trauma is associated with adverse brain development in multiple brain regions that negatively impact emotional and behavioral regulation, motivation, and cognitive function. Molecular aging may contribute to these mechanisms and lead to a premature aging but less than optimal brain maturation process in traumatized children as they become adults.

v. Clinical practice application

vi. Important tools for practice

Understanding the biological effects of maltreatment provides important tools one can useful in practice. Besides self-report instruments to study changes in moods, emotions, and behaviors during psychotherapeutic and/or pharmacological treatments, sleep can be objectively measured using bio-markers such as actographs, which are non-invasive digital monitoring devices that can be worn on the wrist and measure daily activity, sleep awakenings, and sleep efficiency. Other bio-markers that can be used to monitor and tailor treatment and help prevent the negative biological effects of trauma are monitoring measures of heart rate, body mass index, and post-trauma and follow-up salivary cortisol and amylase concentrations as these measures predict PTSD [ 250], and decreasing these levels during treatment may predict remission.

vii. Future directions

The largest contributor to childhood trauma in the USA is family dysfunction; as almost half of child onset mental disorders and about a third of adult onset mental disorders are preceded by child abuse and neglect, and family dysfunction [ 251]. While the mental disorders found in maltreating parents and child victims are serious, they are amenable to prevention and treatment.

Given how detrimental childhood trauma is to an individual's development, more efforts and social resources are needed for prevention. Studies show that child maltreatment is amendable to primary prevention. Child maltreatment prevention programs, such as home visiting [ 252] during an expectant mother's first pregnancy, aimed at addressing mental health and parenting concerns of high-risk new mothers, show great promise in preventing child abuse and neglect. For example, home visiting of an expectant mother by nurses for low-income, at-risk families has been a well replicated strategy for preventing child abuse and neglect[ 253, 254]. Several studies of this Nurse-Family Partnership Program have demonstrated: improved grade-point averages and achievement test scores in math and reading in grades 1 through 3 in children during their age 9 follow-up assessment [ 255]; decreased internalizing symptoms and decreased rates of tobacco, alcohol, and marijuana use along with improved reading and math scores at age 12 follow-up assessment [ 256]; and decreased antisocial behaviors at age 19 follow-up assessment [ 257]. However, a when a parent becomes maltreating, even an intensive program of home visitation by nurses in addition to standard treatment is not enough to prevent recidivism of physical abuse and neglect [ 258]. Maltreated children in foster care showed less self-destructive behavior, substance use, and total risk behavior problem standardized scores and higher grades than maltreated children who were reunified with their biological families when interviewed during their 6th year follow-up[ 259]. These studies indicate that there are two opportunities to break the cycle of maltreatment. The first opportunity is during the expectant parent's first pregnancy, to aid in fostering a loving and caring environment for the parent/child dyad, and to avoid the neurobiological consequences of childhood maltreatment. These types of early prevention programs are cost effective [ 260]. However, if this cannot be done, the second opportunity is to treat victims of maltreatment after the fact.

There are important evidence-based interventions (e.g., trauma-focused cognitive behavior therapy) for the treatment of PTSD and depression [ 261] and for antisocial behaviors in youth with early trauma (e.g., multisystemic therapy [ 262]). Many of these interventions are in other articles within this issue. However, we do not know the long term effectiveness of these programs. We do not have enough professionals trained in evidence-based practices to treat all child victims, and some youth and their families are simply non-complaint with these treatments. Therefore, we still need to understand the neurobiological consequences of chronic stress on a child's developing brain and body so that we can treat the adverse medical and mental health outcomes of early life stress [ 263]. A society that places its focus on an infrastructure of primary prevention would be choosing the less costly option for victims and for itself.

viii. Conclusions

We outlined how childhood trauma has detrimental consequences on the biological stress systems, and cognitive and brain development. Trauma in childhood is costly for its victims and for society. Resilience is not a common outcome of childhood trauma. In a longitudinal study of individuals who had experienced abuse and neglect during childhood, only 22% of those who had been abused or neglected achieved resiliency based on a comprehensive assessment of healthy adult functioning, by the time they reached young adulthood [ 264]. Females who grew up in poverty and were not maltreated were more likely to show resilience [ 264]. While we have some important evidenced-based treatments for child victims, it is in our interest to put in place a national infrastructure of primary child trauma prevention as the less costly option for future victims and for society. Understanding the neurobiological consequences of child trauma will assist in treating child and adult victims, who tend to be more treatment refractory and may have a different endophenotype, than individuals with medical (including mental health) disorders who do not have such histories. Nevertheless, more work is needed to understand the neurobiological consequences of chronic stress on a child's developing brain and body so that we can treat the adverse medical and mental health outcomes of early life stress in those cases (e.g., warfare, natural disasters, child maltreatment) where prevention and effective early intervention may not occur. Such understanding of the neurobiology and genetic influences of child trauma on child development will lead to novel and effective approaches to treatments (e.g., personalized medicine).

​

1. Trauma in childhood is a grave psychosocial, medical, and public policy problem that has serious consequences for its victims and for society.

2. Chronic interpersonal violence in children is common worldwide.

3. Developmental traumatology, the systemic investigation of the psychiatric and psychobiological effects of chronic overwhelming stress on the developing child, provides a framework and principles when empirically examining the neurobiological effects of pediatric trauma.

4. Despite the widespread prevalence of childhood trauma, less is known about trauma's biological effects in children as compared to adults with child trauma histories; and even less is known about how these pediatric mechanisms underlie trauma's short-term and long-term medical and mental health consequences.

Glossary

PTSD

posttraumatic stress disorder

PTSS

posttraumatic stress symptoms

GABA

gamma-amino butyric acid

LHPA

limbic-hypothalamic-pituitary-adrenal

SNS

Sympathetic nervous system

HPA

hypothalamic pituitary axis

LHPA

Limbic-Hypothalamic-Pituitary-Adrenal

CRH

corticotrophin releasing hormone

CRF

corticotrophin releasing factor

ACTH

adrenocorticotrophic hormone

CNS

Central nervous system

mPFC

medial prefrontal cortex

CSF

cerebrospinal fluid

SNPs

Single nucleotide polymorphisms

AVP

arginine vasopressin

BDNF

brain-derived neurotropic factor

PFC

Prefrontal cortex

LC

locus coeruleus

NET

norepinephrine transporter

BDNF

brain-derived neurotropic factor

NSCAW

National Survey of Child and Adolescent Well-Being

Footnotes

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References

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# data[].attributes.attachment_link.title
"The Biological Effects of Childhood Trauma"

# data[].attributes.attachment_link.description
Trauma in childhood is a grave psychosocial, medical, and public policy problem that has serious consequences for its victims and for society. Chronic interpersonal violence in children is common worldwide. Developmental traumatology, the systemic investigation of the psychiatric and psychobiological effects of chronic overwhelming stress on the developing child, provides a framework and principles when empirically examining the neurobiological effects of pediatric trauma.

# data[].attributes.body
In this study we examine the relationship between different measures of risk taking. We are also interested in personality trait (namely dark triad) correlates and predictors. More specifically we focus on the idea that trait Neuroticism moderates the relationship across various measures of risk taking.
https://doi.org/10.1016/j.paid.2020.110450

# data[].attributes.headline
Fear of sexual assault for oneself and others: A gendered perspective from five states

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Fear of sexual assault for oneself and others: A gendered perspective from five states

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1. Will participants’ sexual orientation have any association with rape myth acceptance?           2. Are students who get drunk on a regular basis (weekly or daily) more or less accepting of rape myths than students who do not get drunk on a regular basis (less than weekly)?    3. Are victims of relationship violence,sexual assault, or rape more or less accepting of rape myths?4. Are people who acknowledge contextual sexual assault in fictional rape scenarios more or less likely to accept rape myths?  

# data[].attributes.subject
1. Will participants’ sexual orientation have any association with rape myth acceptance?           2. Are students who get drunk on a regular basis (weekly or daily) more or less accepting of rape myths than students who do not get drunk on a regular basis (less than weekly)?    3. Are victims of relationship violence,sexual assault, or rape more or less accepting of rape myths?4. Are people who acknowledge contextual sexual assault in fictional rape scenarios more or less likely to accept rape myths?  

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https://scholar.utc.edu/cgi/viewcontent.cgi?article=1260&context=mps

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At issue are two key questions:

Do domestic violence perpetrator programmes (DVPPs) actually work in reducing men’s violence and abuse and increasing the freedom of women and children?

How do we hold more perpetrators to account, since even if DVPPs do work, their limited capacity means the majority of men do not access them and criminal justice interventions alone are clearly not creating the change that all stakeholders seek?

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Domestic abuse experienced by young people living in families with alcohol problems: results from a cross-European study

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Domestic abuse experienced by young people living in families with alcohol problems: results from a cross-European study

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Richard Velleman,Lorna Templeton,Danielle Reuber,Michael Klein,Diana Moesgen

https://onlinelibrary.wiley.com/doi/abs/10.1002/car.1047

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Abstract

This paper presents findings from the European Union (EU) DAPHNE project ALC-VIOL (2005-07). The project involved ten EU states (Germany, Austria, England, Finland, Hungary, Ireland, Malta, Netherlands, Poland and Spain). The research involved interviews with young people aged 12-18 from Germany, Poland, Spain, England and Malta on their experiences of living with parental alcohol misuse and parental violence. The children all had parents involved in treatment for alcohol problems. The study highlights the stressful experiences these children underwent, the effects on them, their coping strategies, and the support that they received and/or wished for, and underlines the need for a more coherent approach to help these children. Copyright © 2008 John Wiley & Sons, Ltd.

# data[].attributes.attachment_link.title
Domestic abuse experienced by young people living in families with alcohol problems: results from a cross‐european study

# data[].attributes.attachment_link.description
This paper presents findings from the European Union (EU) DAPHNE project ALC-VIOL (2005-07). The project involved ten EU states (Germany, Austria, England, Finland, Hungary, Ireland, Malta, Netherlands, Poland and Spain). The research involved interviews with young people aged 12-18 from Germany, Poland, Spain, England and Malta on their experiences of living with parental alcohol misuse and parental violence.

# data[].attributes.headline
Measuring Myths about Domestic Violence: Development and Initial Validation of the Domestic Violence Myth Acceptance Scale

# data[].attributes.subject
Measuring Myths about Domestic Violence: Development and Initial Validation of the Domestic Violence Myth Acceptance Scale

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doi.org/10.1080/10926770801917780

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studies suggest that programs including a cognitive component are as twice as more effective in reducing recidivism rates. 

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studies suggest that programs including a cognitive component are as twice as more effective in reducing recidivism rates. 

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https://www-sciencedirect-com.ezproxy.derby.ac.uk/science/article/pii/S1359178913000724

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The aim of the study reported here was exploratory: to capture the views and perspectives of professional stakeholders concerning service provision in the UK for people who have experienced sexual violence and abuse. In particular, we wanted to gain an understanding of how forms of peer support were perceived, in order to provide a foundation for the development of future services.

https://journals.sagepub.com/doi/full/10.1177/08862605211007931

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Why is there  unknown  or  insufficient  field  reliability  of  forensic  procedures?
and
How does experts’  lack of  independence  from  those  requesting  their  services have an affect?

Guarnera, L. A., Murrie, D. C., & Boccaccini, M. T. (2017). Why do forensic experts disagree? Sources of unreliability and bias in forensic psychology evaluations. Translational Issues in Psychological Science, 3(2), 143.

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This study aims to investigate how negative life-events may inﬂuence interviewee performance on the Gudjonsson suggestibility scale (GSS). Moreover, self-esteem will also be investigated in relation to both the experience of negative life-events and interrogative suggestibility

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This study aims to investigate how negative life-events may inﬂuence interviewee performance on the Gudjonsson suggestibility scale (GSS). Moreover, self-esteem will also be investigated in relation to both the experience of negative life-events and interrogative suggestibility

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https://www.researchgate.net/publication/229745477_Interrogative_suggestibility_self-esteem_and_the_influence_of_negative_life-events

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www.researchgate.net needs to review the security of your connection before proceeding.

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Is Campus Rape Primarily a Serial or One Time Problem?

# data[].attributes.subject
Is Campus Rape Primarily a Serial or One Time Problem?

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https://www.jimhopper.com/pdf/foubert_2019.pdf
Research Question 1: What portion of college men commit alcohol-involved sexual assault? Research Question 2: What portion of assault perpetrators commit one versus more than one incident of alcohol-involved sexual assault? Research Question 3: What portion of the total number of alcohol-involved sexual assaults are committed by men who commit two or more sexual assaults? Research Question 4: To what extent do men involved in fraternities commit alcohol-involved sexual assault? Does this differ from other men? Research Question 5: To what extent do men involved in athletics commit sexual assault? Does this differ from other men?

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The impact of ADHD and conduct disorder in childhood on adult delinquency: A 30 years follow-up study using official crime records

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The impact of ADHD and conduct disorder in childhood on adult delinquency: A 30 years follow-up study using official crime records

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https://bmcpsychiatry.biomedcentral.com/articles/10.1186/1471-244x-11-57

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Research article

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BMC Psychiatry 11, Article number: 57 (2011) Cite this article

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Abstract

Background

Few longitudinal studies have explored lifetime criminality in adults with a childhood history of severe mental disorders. In the present study, we wanted to explore the association between adult delinquency and several different childhood diagnoses in an in-patient population. Of special interest was the impact of disturbance of activity and attention (ADHD) and mixed disorder of conduct and emotions on later delinquency, as these disorders have been variously associated with delinquent development.

Methods

Former Norwegian child psychiatric in-patients (n = 541) were followed up 19-41 years after hospitalization by record linkage to the National Register of Criminality. On the basis of the hospital records, the patients were re-diagnosed according to ICD-10. The association between diagnoses and other baseline factors and later delinquency were investigated using univariate and multivariate Cox regression analyses.

Results

At follow-up, 24% of the participants had been convicted of criminal activity.

In the multivariate Cox regression analysis, conduct disorder (RR = 2.0, 95%CI = 1.2-3.4) and hyperkinetic conduct disorder (RR = 2.7, 95% CI = 1.6-4.4) significantly increased the risk of future criminal behaviour. Pervasive developmental disorder (RR = 0.4, 95%CI = 0.2-0.9) and mental retardation (RR = 0.4, 95%CI = 0.3-0.8) reduced the risk for a criminal act. Male gender (RR = 3.6, 95%CI = 2.1-6.1) and chronic family difficulties (RR = 1.3, 95% CI = 1.1-1.5) both predicted future criminality.

Conclusions

Conduct disorder in childhood was highly associated with later delinquency both alone or in combination with hyperactivity, but less associated when combined with an emotional disorder. ADHD in childhood was no more associated with later delinquency than the rest of the disorders in the study population. Our finding strengthens the assumption that there is no direct association between ADHD and criminality.

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Background

Although conduct disorder is a well known antecedent of antisocial development, other childhood disorders as precursors of antisociality are more controversial. So far, long-term follow-up studies have demonstrated that attention-deficit/hyperactivity disorder (ADHD) combined with conduct disorder is a precursor of later antisocial behaviour [ 11- 13]. There are, however, discrepant findings with regard to ADHD without conduct problems as an independent precursor of criminality. Based on the results of long-term epidemiological follow-up studies, Farrington [ 3], Babinski et al. [ 14] and Sourander et al. [ 8] found that hyperactivity-impulsivity, independently of conduct problems, predicted later criminality in males. In two long-term clinical follow-up studies, Mannuzza et al. [ 15, 16] similarly found that ADHD was a developmental precursor of antisocial behaviour in early- and mid-adulthood. Satterfield et al. [ 13], on the other hand, reported in his clinical follow-up study of hyperactive outpatient boys that only those individuals with ADHD combined with childhood conduct problems were at increased risk of criminality. Likewise, in a 10-year follow-up study of a birth cohort, Fergusson et al. found that children with attention deficits but no conduct problems were not at increased risk of juvenile delinquency. They were, however, at risk of later reduced academic success in a dose-response manner [ 17]. Recently, Diamantopolou et al. [ 2], similarly, found that there were no direct association between ADHD symptoms and later antisocial personality problems. Neither did they find that the combination of internalizing and externalizing symptoms appeared to add to the prediction of later antisocial behaviour in adolescence.

During the last decades, there has been a growing interest in the interplay between internalizing and externalizing problems, but there have been no clear findings about the outcome for children with comorbid conduct and emotional disorders. Sourander et al. found that children with combined emotional and conduct problems had a higher risk of criminality compared with children who only had emotional problems, attention deficits and/or conduct problems [ 8]. Their results provided only partial support from previous research. In two longitudinal clinical studies, Harrington et al. [ 18] and Fombonne et al. [ 19] found that children and adolescents with comorbid conduct and depressive disorders had a higher risk of later criminality and antisocial behaviour than those who only had emotional disorders. However, the outcome among children with comorbid disorders was similar to those with conduct disorders alone.

In sum, there are still no consistent findings from epidemiological or clinical studies whether ADHD alone is a precursor of later criminality; nor is it known whether children with combined emotional and conduct disorder are at higher risk of later antisocial behaviour than those with conduct disorder alone or in combination with hyperactivity.

In the present study, former child psychiatric in-patients were followed up 19 to 41 years after hospitalization by linking their records to the National Register of Criminality. The combination of a long follow-up period and diagnostic evaluation, according to the ICD-10 classification system, made this study suited for exploring the association between several different childhood diagnoses and the development of criminality in adolescence and into mid-adulthood. The mean age at follow-up was 38 years, an age after which the likelihood of criminal debut is minimal. We could, therefore, provide a comprehensive picture of lifetime criminality in adults with a childhood history of severe mental disorders.

In addition, the extensive information in the hospital records made it possible to control for vulnerability factors, other than diagnoses, that could contribute to the development of later criminality.

We wanted to test the hypothesis that there was a direct association between hyperkinetic symptoms and later criminality in former child psychiatric in-patients, with ADHD increasing the risk for delinquency, independent of conduct disorder comorbidity or not.

We also wanted to test the hypothesis that former child psychiatric in-patients with mixed disorder of conduct and emotions were at increased risk for later criminality compared to those with conduct disorder only. A final issue was to explore whether vulnerability factors other than diagnoses could enhance prediction of delinquent outcome.

Methods

Procedure

All consecutively admitted in-patients to the children's unit at the National Centre for Child and Adolescent Psychiatry (NCCAP), in Oslo Norway, from January 1968 to October 1988, were included in the study (n = 635). With regard to ethnicity, all but ten were Caucasians. The NCCAP's children's unit, which was opened in 1968, provided specialized treatment for children 13 years or younger from all over Norway who had complex child psychiatric disorders in need of skilled treatment. The hospital records provided detailed baseline information of behaviour and symptoms, psychological test results, school performance (all children of school age had adjusted school programmes during their hospitalization) and extensive anamnestic information about the children and their families. The study population was identified from the population register at the Central Bureau of Statistics, by using the citizen's identity number, which ensured a definite identification. The patient group was matched with the National Register of Criminality at follow-up in July 2007. The criminal register has lifetime information about all criminal proceedings against everyone residing in Norway. The reported findings are based on court convictions for infractions of all breaches of the law. The terms "delinquent", "criminal" and "convicted" are used interchangeably in this paper.

Age at first and last entry into the register was recorded, together with a description of the offences committed. The offences were classified into violent offences (all offences involving interpersonal aggression and threats, robbery, arson), sexual offences (offences against public decency, immoral intercourse with minors, incest, rape), crimes against property (larceny of all kind, frauds, forgery, embezzlement), drug violations and "other offences" (traffic offences, vandalism, possession of weapons, refusal to obey orders, vagabonding, crimes against military law). The sentences were categorized in terms of judicial fine only, conditional imprisonment, unconditional imprisonment and mandatory care. Under the Norwegian criminal code, people with mental retardation are able to stand trial. People with mild mental retardation (IQ between 70-55) can be sentenced to ordinary prisons. Offenders in the category of severe mental retardation (IQ below 55) are seldom prosecuted, but can be sentenced to mandatory care for a period of 3 years [ 22].

Participants

For 635 in-patients admitted to hospital, 78 of the hospital records could not be located. In one case, the record was incomplete, and another patient who was older than 13 years at admission was excluded. In five cases, we could not determine the personal identification number at the Central Bureau of Statistics.

A total of 550 subjects (87% of the original sample) were identified in the population register at the Central Bureau of Statistics at follow-up in 2007. Of these, 25 (5%) had died and 14 (3%) had emigrated. Those who had emigrated or died before the age of 14 years (n = 9), which was the legal age of criminal responsibility at that time, were excluded from the study. Thus, a total of 541 participants were included in this study.

The sex distribution was 366 (68%) boys and 175 (32%) girls, and the mean age at hospitalization was 7.9 years (SD 2.7, range 0-13).

The mean age at follow-up (when those who had emigrated or died were excluded) was 38.3 years (SD 7.0, range 23-52), and the mean follow-up period from first admission was 30.4 years (SD 6.6, range 19-41).

With regard to treatment, 57% of the patients were admitted to the family ward, where the intervention was based mainly on diagnostic evaluation and family therapy. The other patients, who were admitted to the inpatient long-term ward (40%) and to the day care ward (3%), received diagnostic evaluation, psychodynamic-oriented individual therapy and/or social psychiatric interventions. The mean length of stay was 1.1 months at the family ward, 8.2 months at the inpatient long-term ward and 22.5 months at the day care ward. In total, 24% of the in-patients were admitted more than once.

Measures

Mental health (ICD-10)

Based on all the information in the hospital records, including weekly ward descriptions of the children, all the patients were re-diagnosed according to current criteria in ICD-10 [ 23]. The hospital records were comprehensive with extensive anamnestic information provided by parents, teachers and local health workers. All 541 patients were re-diagnosed by the first author and independently by at least one other experienced child psychiatrist. If the two raters disagreed, the case was discussed by a research group of four child psychiatrists, and a consensus diagnosis was established.

It was found that 25% of the patients had more than one psychiatric ICD-10 diagnosis, with nonorganic eneuresis or encopresis being the co-diagnoses most often encountered (59% of the cases). The diagnosis of greatest clinical importance (principal diagnosis) was pre-empted in this study. Table 1 contains a summary of the principal diagnoses, which were clustered into 10 groups: 1) Conduct disorder (F91); 2) Disturbance of activity and attention/ADHD (F90.0), (in accordance with ICD-10 diagnostic criteria, they all fulfilled the DSM-IV criteria for the corresponding ADHD of combined type, except for five participants who fulfilled the criteria for ADD); 3) Hyperkinetic conduct disorder ((F90.1), the criteria for both hyperkinetic and conduct disorders must be met to achieve the diagnosis); 4) Mixed disorder of conduct and emotions ((F92), the criteria for both an emotional disorder and a conduct disorder must be met to achieve the diagnosis); 5) Emotional disorder, including emotional disorders in childhood (F93), anxiety and other neurotic disorders (F40-F49), mood disorders (F30-F39), eating disorders (F50) and mutism (F94.0); 6) Attachment disorder (F94.1 and F94.2); 7) Pervasive developmental disorder (PDD) (F84); 8) Mental retardation only (MRO) (F70-F79 as the only diagnosis); 9) Other disorders, including organic mental disorders (F06), tic disorders (F95), nonorganic eneuresis (F98.0), encopresis (F98.1), stuttering (F98.5) and psychosis (F20); and 10) Z-group diagnoses including diagnoses given for factors influencing health status and contact with health services. Investigations of problems within the family usually led to such a diagnosis. Descriptions of the child's symptoms did not meet the criteria for a psychiatric diagnosis.

Table 1 Distribution and descriptive characteristics of diagnostic groups at admission

Socio-demographic variables

Gender was registered at baseline and reported in table 1.

We also applied a global assessment of chronic family difficulties (CFD) [ 24] based on all the information available in the hospital records of the past and present family situation. Socioeconomic conditions, social network, marital or family discord and current/previous physical and mental health of the family members were recorded. The total burden of difficulties was scored on an interval scale from 0 to 6. A score of 0 reflects no sign of chronic family difficulties and a score of 6 reflects severe difficulties/very disturbed family environment (Table 1).

Level of cognitive abilities

Children's Global Assessment Scale (CGAS)

The children were also reassessed on the CGAS, a global assessment of the child's psychosocial functioning [ 27]. The scale runs from 1 to 100, with 1 indicating the most severely disordered and 100 the best functioning child. The assessment was based on the child's functioning at admission (Table 1).

Inter-rater reliability study

An inter-rater reliability study was carried out for 476 patients, yielding an overall kappa value of 0.77 for the ICD-10 diagnoses in Table 1 (varying from 0.52 for attachment disorders to 0.89 for PDD and mental retardation), and intraclass correlation coefficients (ICC) of 0.83 for CGAS, 0.86 for CFD and 0.85 for cognitive level.

Statistical methods

Descriptive statistics are presented as means with standard deviations, medians and ranges, as appropriate. Variables were investigated using Student's two-sample t test for continuous variables, and Pearson's chi-square test and Fisher's exact test for categorical variables. Cox proportional regression analyses were used to analyse the risk of later convictions. In these analyses, participants were followed from the age of 14 years, which was the youngest age for registration of criminality, until their first contact with the police, or otherwise, their date of emigration, death, or else their follow-up in July 2007 for those who had not been convicted. The effects of possible prognostic variables were tested using univariate Cox regression. Variables that were significant at the 5% level were included in a multivariate Cox regression analysis. Hazard ratios, which were used as measures of relative risk, are presented together with their 95% confidence intervals.

Kappa statistics and intraclass correlation coefficients (ICC) analyses were used to examine the inter-rater reliability.

SPSS version 15 was used for the statistical analyses.

Ethics

The study was approved by the Regional Committee of Ethics in Medical Research, the Department of Health and Social Services and the Norwegian Data Inspectorate.

Results

Crime rates

Of the total sample of 541 persons, 131 (24%) were found in the crime registry at follow-up (Table 2). Of these, 114 (31%) of the males and 17 (10%) of the females had been convicted. Of the 131 individuals who committed crimes, 85 (65%) were re-offenders.

Table 2 Vulnerability factors for delinquency.

Although the crimes were of different types, they all showed extensive overlap (Figure 1). Most offenders had committed crime against property (n = 88, 67%), followed by drug offences (n = 56, 43%) and violent offences (n = 54, 41%). The mean number of sentences was 4.7 (SD 5.5, range 1-35), and the median was 2.0.

Distribution and overlap of the various crimes committed in the convicted group, n = 131. ª : 9 sexual offences, 4 of these sexual offences only. ( )* = in combination with "other crimes". (Ex: 10 (2)*= 2 of ten offences in combination with "other crimes".) Those committed only "other crimes" (n = 14), are excluded from the diagram.

Fifteen (11%) participants, who had only received judicial fines, had committed a variety of crimes. Those receiving unconditional or conditional sentences were significantly younger at their first offence than those who only received judicial fines (20.1 years; SD 5.9, range 14-46 years, vs. 25.7 years, SD 6.8, range 16-37 years, p < 0.01).

None of the offenders was sentenced to mandatory care.

Childhood precursors of convictions for delinquency

Table 2 shows the relationship between possible vulnerability factors recorded at baseline and convictions recorded at follow-up. Results from univariate and multivariate analyses performed are presented.

Three child psychiatric disorders were positively associated with a criminal act in the univariate Cox regression analyses (Table 2). Conduct disorder (56% convicted, RR = 3.2, 95% CI = 2.0-4.9), hyperkinetic conduct disorder (54% convicted, RR = 3.4, 95% CI = 2.2-5.2) and mixed disorder of conduct and emotions (33% convicted, RR = 1.6, 95% CI = 1.1-2.5) represented significantly higher risk of later criminality when compared with the other mental disorders. The diagnoses of PDD (6% convicted, RR = 0.2, 95% CI = 0.1-0.4) and MRO (3% convicted, RR = 0.1, 95% CI = 0.0-0.9) significantly reduced the risk of future criminal behaviour. Male gender (31% convicted, RR = 3.8, 95% CI = 2.3-6.3) and CFD scale score (RR = 1.4, 95% CI = 1.2-1.6) were other vulnerability factors representing higher risk of later criminality, while MR (9% convicted, RR = 0.2, 95%CI = 0.1-0.4) represented lower risk of later criminality. All but one of the eight associated factors were entered into a Cox regression. Because the MRO variable represented overlapping constructs with the overall MR variable, it was not included in the equation. Six variables remained significant in the final multivariate model (Table 2): Conduct disorder (RR = 2.0, 95%CI = 1.2-3.4), hyperkinetic conduct disorder (RR = 2.7, 95% CI = 1.6-4.4), male gender (RR = 3.6, 95%CI = 2.1-6.1) and CFD scale score (RR = 1.3, 95% CI = 1.1-1.5) represented higher risk for later delinquency. The diagnosis of PDD (RR = 0.4, 95%CI = 0.2-0.9) and MR (RR = 0.4, 95%CI = 0.3-0.8) reduced the risk for later conviction.

We found no evidence of interactions. We specifically found no interaction between cognitive level and ADHD or between CD and chronic family difficulties (data not shown).

We also forced the ADHD variable into the final model. The results of main vulnerability factors did not change (data not shown).

Because a significant proportion of the participants had mental retardation (n = 170), and because the cognitive level was different between diagnostic groups (Table 1), separate Cox analyses were used to evaluate those with normal cognitive abilities. We found the relative strengths of the main vulnerability factors for criminality to be similar (data not shown). We also ran analyses where sub-grouping of mental retardation was more fine-meshed, and where those with severe mental retardation (n = 73) were excluded, without changing the results of main vulnerability factors (data not shown).

Because few of the females had been convicted (n = 17), and because the gender distribution was different between diagnostic groups (Table 1), separate Cox analyses were also performed exclusively for males. In the multivariate Cox regression analyses, all the main vulnerability factors remained significant (data not shown).

Finally, when the five children in the ADHD group that only fulfilled the criteria for ADD were excluded from the ADHD group, the results remained the same. There was still no association between ADHD and delinquency.

Discussion

In the present study, 131 (24%) individuals had committed crimes during the follow-up period and were found in the crime registry. We found conduct disorder and hyperkinetic conduct disorder in childhood to be highly associated with delinquency in adulthood. When conduct disorder was combined with emotional disorder, the association was no longer significant, and there was no direct association from ADHD in childhood to future delinquent behaviour. Thus, our two hypotheses were not confirmed. A high chronic family difficulties scale (CFD) score enhanced prediction of future criminality.

Crime rate

The crime rate in our child psychiatric in-patient population was 24%. It is difficult to obtain reliable figures concerning the prevalence of convicted persons in Norway, but estimates indicate close to 10% [ 28]. Recently, in a Norwegian birth cohort from 1977, about 10% (16% males and 3% females) were charged for a crime before the age of 25 years [ 29]. Our findings, thus, indicate a substantial increased criminal activity in the study population compared to the general population. The increased crime rate is similar to findings in a Swedish register study of child psychiatric in-patients, 18 years or younger, of whom 21% had received sentences for criminal offences at follow-up when they were from 33 to 37 years old [ 30]. The delinquency rate was even higher (52%) in a long-term follow-up study of former adolescent psychiatric in-patients conducted by Kjelsberg et al. In this study, 1276 patients aged from 12 to 18 years were followed up 15-33 years after hospitalization [ 28]. Engqvist and Rydelius [ 31] found, likewise, in their study of former child and adolescent psychiatric patients, that 44% of the 279 in-patients were contained in the crime register at follow-up. The lower crime rate in our group might be due to its heterogeneous diagnostic distribution, there being a significant proportion of participants with PDD (21%). Many of our participants had cognitive level below 70 (n = 170, 31%), and when they were excluded, the crime rate in our population increased to 32%. However, regardless of these study populations being different, the main conclusion is the same: Former child and adolescent psychiatric patients are at increased risk for development of future delinquency compared to the general population.

Childhood precursors of convictions for delinquency

Mental health (ICD-10)

Conduct disorder and hyperkinetic conduct disorder independently represented high risks of later court convictions. Our findings reinforce an already extensive body of research that has documented the association between early conduct problems and later delinquency [ 3, 11, 13, 31- 33], and give support to the assumption that conduct disorder, as an antecedent, should be a priority prevention target. For those children who met criteria for both conduct disorder and ADHD, this did not tend to add substantial to the prediction of future criminality. This is in line with Lahey et al. [ 34], who found no elevated risk for later antisocial problems among children who met criteria for both conduct disorder and ADHD compared to children with conduct disorder alone. However, this issue is controversial, with research showing discrepant findings [ 34, 35], and should be further explored in future research on larger populations than the present one.

The above mentioned findings are in many ways difficult to reconcile because the relevant studies discussed have used different designs (epidemiological vs. clinical), different classification systems (DSM-IV vs. ICD-10 vs. dimensionally scored symptoms) and different outcome measures (conviction rate, self-reported crime, antisocial personality disorder). In some of the studies [ 15, 16] oppositional defiant disorder (ODD) was not an exclusion criteria for children with ADHD, which in turn may have increased the risk for later criminality in these ADHD groups.

Our findings partly support both of the contradictory assertions mentioned above. We did not find elevated risk for convictions among individuals with ADHD when compared to other child psychiatric patients, but the crime rates for children with ADHD seemed to be elevated compared to a crude estimate in the general population. Because the comparison group in this study was referred in-patients with other diagnoses than ADHD, our findings apply only to differences among in-patient children who received different diagnoses. Longitudinal studies including large groups of children with ADHD matched with symptom-free control groups have to be conducted in order to address the question of whether ADHD alone predicts criminality. Nonetheless, previous research has found a linear association between the number of behavioural problems and later antisocial problems [ 34, 36]. All our children were severely affected in-patients with extensive symptom load and with low psychosocial functioning. Thus, our finding, that ADHD did not predict subsequent delinquency, should strengthen the assumption that there is no direct association between ADHD and later criminality.

However, early hyperkinetic symptoms have been reported to enhance the development of early onset CD [ 35]. Our findings thus illuminate the importance of target intervention in the ADHD group, to prevent development of comorbid conduct disorder, which has been claimed to be the mediator between ADHD and criminality [ 32].

Sociodemographic variables

Well known risk factors such as male gender and family adversities [ 3, 28, 37] were also in this study associated with later delinquency. We used the chronic family difficulties scale (CFD) score to assess the family adversities. A high CFD total score, representing an accumulation of unfavourable psychosocial background factors (e.g. low family income, poor social network and parental psychopathology), significantly predicted future criminality (p < 0.01).

Factors reducing the risk of delinquency

As demonstrated in other studies, PDD and mental retardation appeared to protect against delinquency [ 26, 40]. This is not unexpected considering the overlap between the PDD group and those with mental retardation (66% of the PDD population had mental retardation), and that mentally retarded and autistic people are often raised in protected environments at home or in institutions. Besides, individuals with severe mental retardation are seldom prosecuted for violation of the law, although, according to the penal code, they can be sentenced to mandatory care. Thus, the strong negative association between cognitive disabilities and convictions found in this study may therefore be an artefact of such practices. Worth mentioning, when those individuals with severe mental retardation were excluded from the material, mental retardation still remained protective, which means that having a mild mental retardation also seemed to reduce the risk for criminality in our population. The strong negative association between PDD and convictions was found regardless of exclusion of those with comorbid mental retardation. This strengthens the finding of reduced risk for delinquency in this group regardless of intellectual level, but may still be due to close monitoring of these individuals in protected environments.

Strengths and limitations

In this study, data were collected over a period varying from 19 to 41 years (the mean follow-up period was 30 years) in a longitudinal follow-up study to examine the link between psychiatric disorders in childhood and later delinquency. The study's strengths are the long follow-up interval and the large number of patients included, combined with the high proportion of patients traced at follow-up (87%). The outcome measures are robust official records data. To a certain extent, the study's design can be regarded as quasi-prospective because the data were collected from the hospital records before the outcome were obtained from official records.

The study has several limitations. All information was based on hospital records; these are not always reliable scientific sources. However, the hospital records were of good quality giving a detailed and thorough description of the patients' symptoms, scholastic skills and childhood circumstances. The re-diagnosis and scoring of the data from the study sample were completed by experienced psychiatrists. Inter-rater reliability was high, in line with previous research, where validity of file-based diagnostic ratings has been found satisfactory [ 41, 42].

The study population is not representative of child psychiatric patients in general. Because these in-patients represented severe cases that might represent a worsening of the long-term outcome, factors identified in this study should only be interpreted as vulnerability factors within a psychiatric in-patient population. However, we have confidence in the findings because they replicate results from other studies with different populations. Results obtained from multivariate regression analyses should always be interpreted with caution, and the factors identified should not be interpreted as causative factors.

The study considered only sentenced criminality. This probably underestimates the antisocial activity, perhaps especially among those individuals with severe mental retardation which often are exempted from criminal prosecution. However, the use of official crime records ensured that only criminal acts severe enough to elicit sanctions from the justice system were included, and bias in self-reported offending were avoided.

Generalization of the findings is limited to nations with similar criminal judicial systems.

Finally, our small group of convicted females provided insufficient statistical power to predict delinquent behaviour in females exclusively.

Conclusions

Our results indicate that it seems possible to identify children with a high risk of developing delinquency. The crime rate in this study of former child psychiatric in-patients was more than twofold that of the general population. We found conduct disorder alone or in combination with hyperactivity in childhood to be highly related to delinquency in adulthood. Our controversial finding, that conduct disorder combined with emotional disorder was less associated than conduct disorder alone, should be addressed in future research. We found chronic family difficulties to predict future criminality. Taking both diagnosis and family difficulties into account could enhance the prediction of future delinquency.

Interestingly, children with ADHD in the absence of conduct disorder had no higher risk for later delinquency than the rest of the study population in the present study. As these children had extensive symptom load, our finding strengthens the assumption that there is no direct association between hyperkinetic symptoms and criminality.

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Acknowledgements

We gratefully acknowledge Eili Sponheim, Ingrid Spurkland and Inger Helene Vandvik for their participation in recoding hospital records and for their crucial role in initiating and supporting the accomplishment of the study.

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Authors and Affiliations

1. Division of Mental Health and Addiction, Oslo University Hospital, Norway

Marianne Mordre & Anne Margrethe Myhre

2. Institute for Clinical Medicine, University of Oslo, Norway

Berit Groholt & Anne Margrethe Myhre

3. Centre for Forensic Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital, Norway

Ellen Kjelsberg

4. Unit of Biostatistics and Epidemiology, Oslo University Hospital, Norway

Berit Sandstad

Corresponding author

Correspondence to Marianne Mordre.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

All authors (except BS) conceived of and designed the study. MM participated in the collection of data, performed statistical analyses and drafted the first manuscript. BG participated in the collection of data, helped with statistical analyses and made significant contribution to the final draft. BS made significant contribution to the statistical analyses and critically reviewed the manuscript. EK made significant contribution to the final draft. AMM participated in the collection of data, made significant contribution to the final draft and supervised the work and critically reviewed the manuscript. All authors read and approved the final manuscript.

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Mordre, M., Groholt, B., Kjelsberg, E. et al. The impact of ADHD and conduct disorder in childhood on adult delinquency: A 30 years follow-up study using official crime records. BMC Psychiatry 11, 57 (2011). https://doi.org/10.1186/1471-244X-11-57
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Keywords

Antisocial Behaviour

Crime Rate

Conduct Disorder

Pervasive Developmental Disorder

ADHD Group

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The impact of ADHD and conduct disorder in childhood on adult delinquency: A 30 years follow-up study using official crime records - BMC Psychiatry

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Background Few longitudinal studies have explored lifetime criminality in adults with a childhood history of severe mental disorders. In the present study, we wanted to explore the association between adult delinquency and several different childhood diagnoses in an in-patient population.