Rutter's Child and Adolescent Psychiatry Book 2

637 Author Top-down studies Weissman et al. (1984) Turner et al. (1987) Rende et al. (1995) Warner et al. (1995) Capps et al. (1996) Beidel & Turner (1997) Merikangas et al. (1999) Biederman et al. (2001) McClure et al. (2001) Biederman et al. (2004) Pine et al. (2005a) Author Bottom-up studies Last et al. (1991) Lieb et al. (2000) Parental diagnoses: AGO, agoraphobia; MDD, major depression; OCD, obsessive compulsive disorder; PD, panic disorder. Offspring diagnoses: AD, anxiety disorder including PD, OCD or social phobia; GAD, generalized anxiety disorder; OAD, overanxious disorder; SAD, separation anxiety disorder. T1, time one; T2, 2-year follow-up. * 95% Confidence interval of odds ratio excludes 1.0 (i.e., statistically significant at P ≤ 0.05). Parental diagnosis (No of offspring) MDD and PD (19) (mothers) MDD (23) (mothers) OCD or AGO (16) Dysthymia (14) MDD (164) No MDD (68) MDD (32) MDD and PD (60) PD (17) AGO (16) AD (28) MDD (24) AD and MDD (29) AD, AGO and OAD (36) PD and MDD (141) MDD (46) PD (26) No PD or MDD (99) Anxiety, no MDD (40 in mother) MDD, no Anxiety (248 in mother) Anxiety and MDD (110 in mother) PD and MDD (56) MDD (132) PD (55) No PD or MDD (491) PD and MDD (41) MDD (53) PD (24) No PD or MDD (26) Children’s diagnoses (No of mothers) SAD (19) OAD (22) OAD and SAD (17) SoPh (n = 58) Odds ratio between parental psychopathology and anxiety disorders in offspring vs. normal controls 10.4* 2.3 7.2* 5.5* 2.2 T1*; 2.9 T2* 0.92 T1; 0.92 T2 2.5* 1.1 2.3* 3.9* 5.4* 5.7* 5.4* 2.5 (≤2 anxiety disorders) 8.2* 4.3 8.8* – 3.1* (anxiety in child) 1.6 (anxiety in child) 3.6* (anxiety in child) (≤2 anxiety disorders) 2.3* (anxiety in child, PD in parent) 1.3 (anxiety in child, MDD in parent) 4.9* (anxiety in child, PD in parent) 4.8* (anxiety in child, MDD in parent) Odds ratio between parental psychopathology and anxiety disorders in offspring vs. normal controls With PD in 1.4 (SAD in child) Parents 4.2* (OAD in child) 10.7* (OAD & SAD in child) With SoPh 4.7* (parent SoPh) in child 3.5* (parent other anxiety) 3.6* (parent depression) Table 39.2 Anxiety in children as a function of parental psychopathology. 9781405145497_4_039.qxd 29/03/2008 02:52 PM Page 637

of anxiety, complicates clear interpretation of the nature of transmission. As noted in chapter 23, the identification of genes will contribute greatly to our understanding of causal factors. No genomic studies have been conducted in childhood anxiety disorder. In adults, panic disorder, which has been shown to be familial, has been examined for influential genes. Replications have failed. Some suggest that it is futile to expect nosological clarity in psychiatry from genetic findings (Kendler & Greenspan, 2006). It is unlikely that the search for genes in childhood anxiety disorders will fare better than it has for adult anxiety disorders. This failure will limit definitive statements regarding the exact nature of genetic influences, but it will not alter the need to rely on other informative clinical and biological strategies to determine the nosological validity of childhood anxiety disorders. Endophenotypes Research has begun to move beyond examination of familial aggregation in anxiety symptoms to the study of underlying mechanisms. Anxiety is viewed as a downstream manifestation of genetically based perturbations in neural function that do not directly map on to diagnostic categories. Rather, they cause abnormalities in information processing that lead to psychopathology. The term “endophenotype” has been used to describe heritable abnormalities in neural function and associated information-processing capacities (Gottesman & Gould, 2003). Endophenotypes show independent associations with psychiatric disorders and with their risk factors. Strong evidence for potential endophenotypes is scarce; working memory abnormalities in schizophrenia probably represent the most compelling example in psychiatry. Three lines of work provide preliminary data on potential endophenotypes in pediatric anxiety disorders. First, behavioral inhibition has been conceptualized as an endophenotype. Longitudinal studies note associations with anxiety disorders, and family studies with parental panic disorder (Kagan, Snidman, McManis et al., 2001). This work views temperament and anxiety as alternative manifestations of perturbations in the brain’s fear circuit. However, because behavioral inhibition may also be associated with parental depression, there may not be diagnostic specificity in this relationship (Caspi, Moffitt, Newman et al., 1996; Rosenbaum, Biederman, Hirshfeld-Becker et al., 2000). In addition, some suggest that behavioral inhibition represents manifest psychopathology, as opposed to a risk factor or endophenotype. An intervention study found stronger treatment effects on anxiety symptoms than on behavioral inhibition (Rapee, Kennedy, Ingram et al., 2005), supporting the endophenotype perspective for behavioral inhibition. Second, some work implicates enhanced autonomic reactivity in risk for anxiety (Grillon, Dierker, & Merikangas, 1997; Merikangas, Avenevoli, Dierker et al., 1999). As with behavioral inhibition, reactivity-based endophenotypes are presumed to result from perturbations in fear-circuit function. Particular interest has focused on measures of hypothalamic–pituitary– adrenal (HPA) axis activity, although such findings in pediatric anxiety disorders are inconsistent (Terleph, Klein, RobersonNay et al., 2006). Third, information-based approaches suggest that abnormal attention regulation during threat exposure may represent an endophenotype (Pine, Klein, Roberson-Nay et al., 2005b). Attention-processing abnormality to threat, also presumed to result from fear-circuit dysfunction, has been linked to both pediatric anxiety disorders and parental panic disorder. Molecular Genetics Studies of molecular genetic correlates have extended the modern view of psychopathology as the result of circuitrybased perturbations in information processing. Perspectives on psychiatric genetics have advanced considerably in the past 10 years, to the point where most common forms of psychopathology, including pediatric anxiety disorders, are viewed as so-called “complex disorders.” Such conditions are caused by panoplies of genetic and non-genetic factors, each making relatively small contributions to the phenotype. In anxiety disorders, the most productive research has attempted to link specific genetic polymorphisms to neural and cognitive dysfunction. Virtually all work on anxiety is of adults. Current findings implicate a polymorphism of the serotonin transporter gene in fear-circuitry dysfunction (Hariri, Mattay, Tessitore et al., 2002). Other work, again largely in adults, suggests that such genetically based perturbations predispose to psychopathology through interactions with environmental risk (Caspi, Sugden, Moffitt et al., 2003). Although much of this work examines associations with adult depression, it is relevant to pediatric anxiety disorders, given their associations with adult depression. Two studies have reported a gene– environment interaction with the serotonin transporter in pediatric depression (Eley, Stirling, Ehlers et al., 2004; Kaufman, Douglas-Palumberi, Houshyar et al., 2004), and another found such an interaction for behavioral inhibition (Fox, Nichols, Henderson et al., 2005). Behavioral inhibition also has been linked to a polymorphism in the gene for corticotropin-releasing factor (CRF), a key regulator of HPA function (Smoller, Yamaki, Fagerness et al., 2005). Such an association is consistent with data implicating HPA axis function in fear-circuit activity (see p. 639). Psychobiology Neural Circuitry in Animals Advances in basic science have altered theories of anxiety disorders. They are viewed as reflecting individual differences in neural function: pediatric anxiety disorders are hypothesized, by some, to result from abnormalities in physiological systems implicated in animal models of anxiety (Gross & Hen, 2004). This view has led investigators to target various physiological systems in an effort to document psychobiological substrates of anxiety. Animal models of anxiety benefit from strong cross-species conservation in brain circuitry and pharmacology. Distinct CHAPTER 39 638 9781405145497_4_039.qxd 29/03/2008 02:52 PM Page 638

forms of fear are regulated by inter-related brain systems involving the prefrontal and medial temporal lobes. Perhaps the best understood phenomena are learned fears, which can be modeled by “fear conditioning” experiments, where an aversive stimulus, such as a shock, is paired with a neutral stimulus, such as a light. Following such pairings, an organism exhibits fear of the formerly neutral stimulus. Learned fear depends upon a neural circuit involving the amygdala, a bilateral collection of individual nuclei located within the brain’s medial temporal lobes (LeDoux, 2000). Learning to fear a previously harmless stimulus involves changes in neural function within the basolateral nucleus of the amygdala, and expression of this learning involves output through the central nucleus. Similarly, the process of extinction, whereby a feared stimulus no longer elicits a fear response, requires communication between the amygdala and frontal cortex, and perturbations in extinction reflect aberrant communication between these regions (Quirk & Gehlert, 2003). Other forms of fear develop without prior learning and are regulated by distinct but related neural circuits. For example, nocturnal organisms such as rodents fear well-lit environments (Davis, 1998). Unlike learned fears, this fear does not extinguish and may actually increase with repeated exposure. Unlearned fear involves the basolateral but not the central nucleus of the amygdala; the two circuits are regulated by distinct neurochemical systems. For example, infusions with CRF may potentiate unlearned fear, but not conditioned fear. Neural Development and Fear The mature fear circuit reflects long-term influences of earlylife rearing environment. A wealth of investigations with rodents shows that alterations in maternal care produce long-term changes in the threshold for engaging the medial temporal lobe and prefrontal components of the fear circuit (Meaney, 2001). These effects arise through non-genomic influences, involving DNA methylation. Specifically, functional aspects are altered for genes involved in regulation of the medial temporal lobe and frontal cortex. Work in non-human primates demonstrates comparable associations between rearing and threat responses (Suomi, 2003). These influences appear also for indices of HPA axis function, generating interest in the relationship between HPA axis function and pediatric anxiety disorders. Much of the scientific interest in rearing effects was based on the implicit assumption of permanent scarring. However, the influence of early life experiences is complicated. For example, over 900 genes are regulated by maternal care (Weaver, Meaney, & Szyf, 2006). Moreover, some effects of rearing on genes are reversible. Further complicating an understanding of effects of early rearing, Mathew, Coplan, Smith et al. (2002) not only failed to replicate increased cerebrospinal fluid (CSF) corticotropin releasing factor (CRF) in primates raised under stress, but obtained diametrically opposite results (Mathew, Coplan, Smith et al., 2002). In sum, the effects of early maternal behavior and stress on later functions are highly complex, indirect and not regularly irreversible. Another approach uses anatomic, neurochemical and genetic manipulation to demonstrate developmental plasticity in the fear circuit. Lesion studies in non-human primates find distinct effects of amygdala lesions on fear-related behaviors in mature relative to immature primates (Amaral, 2002). Genetic and chemical manipulations in rodents produce long-term alterations in fear-related behaviors and associated neural circuitry among immature mice, but not in mature mice exposed to the same manipulations (Gross & Hen, 2004). Altogether, animal data suggest that function of the mature fear circuit reflects influences during childhood on fear-circuit development, but the nature of these influences is likely to be highly complex. Human Physiology and Neural Circuitry Functional aspects of brain circuits that regulate learned and innate fears can be elicited reliably in lower mammals as well as humans, through changes in physiological indices; of these, the startle reflex has the best understood neuroanatomic circuit. The reflex is augmented by presentations of mildly stressful stimuli. The neural circuit involved in fear conditioning in rodents is thought to mediate augmentation of this reflex in humans. Adults with various forms of anxiety exhibit startle abnormalities (Grillon, 2002; Grillon & Baas, 2003). Asymptomatic children of parents with anxiety disorders also have been found to have abnormalities in startle regulation (Grillon, Dierker, & Merikangas, 1997, 1998). Problematically, startle abnormalities reported in at-risk offspring have not been found in youth with anxiety disorders. In addition, startle abnormalities occur in offspring at risk for anxiety and for depression as well, raising questions about the specificity of associations between abnormal startle and anxiety (Grillon, Warner, Hille et al., 2005). Kagan, Snidman, McManis et al. (2001) suggested that behavioral inhibition, a marker of risk, results from abnormalities in the same brain circuits implicated in startle potentiation, based on peripheral physiological profiles, using indices influenced by circuits that regulate fear in mammals. In spite of parallels in neural circuits of fear regulation in humans and animals, there are crucial pharmacological inconsistencies. For example, medications effective in panic disorder do not affect fear conditioning, although they appear to affect certain forms of unlearned fear (Blanchard, Griebel, Henrie et al., 1997; Cassella & Davis, 1985). Moreover, associations between fear conditioning and clinical anxiety disorders are marginal at best (Lissek, Powers, McClure et al., 2005). Accordingly, risk for anxiety disorders has been hypothesized to relate to failures in extinction, or to inherited tendencies to respond to innate unlearned fearful stimuli, rather than to abnormalities in fear-learning per se. The most developed line of research examines respiratory dysregulation in panic disorder (Klein, 1993, 1996). Much like a well-lit room for a rodent, respiratory stimulants represent unlearned fear-inducing stimuli for air-breathing organisms, including humans. A wealth of evidence suggests that sensitivity to respiratory stimulants identifies individuals with a ANXIETY DISORDERS 639 9781405145497_4_039.qxd 29/03/2008 02:52 PM Page 639

diathesis for types of anxiety closely related to spontaneous panic attacks. For example, adults with panic disorder have enhanced responses to respiratory stimulants, such as CO2, sodium lactate, cholecystokinin or doxapram. Sensitivity to CO2 has also been found in children with anxiety disorders, specifically separation anxiety disorder, but not those with social anxiety disorder (Pine, Klein, Roberson-Nay et al., 2005a). Syndromes such as subclinical panic disorder that have strong familial associations with panic disorder are also characterized by enhanced responses to respiratory stimulants. Moreover, in adults, signs of respiratory abnormalities, such as enhanced sensitivity to CO2, occur especially among panic patients with high familial loading (Horwath, Adams, Wickramaratne et al., 1997). In addition, healthy adult first-degree relatives of panic patients also exhibit enhanced responses to respiratory stimuli (Coryell, Fyer, Pine et al., 2001); however, CO2 sensitivity was not found among offspring at risk for panic disorder (Pine, Klein, Roberson-Nay et al., 2005a). Cognition and Anxiety Cognitive processing, specifically memory and attention, is preferentially mobilized by perceived threats, presumably due to the responses’ adaptive value. Brain imaging which has been used to delineate fear-circuit dysfunction in anxiety susceptibility has focused on threats’ abilities to disrupt strategic control of attention or attention orienting (Davis & Whalen, 2001). Two procedures have been common to probe threatrelated effects on cognitive processes in humans. One relies on the “emotional Stroop test,” which taps disruption of strategic attention control. Latencies increase when naming colors of “threat” words as opposed to “neutral” words (Williams, Mathews, & McLeod, 1996). Adults with various anxiety disorders show relatively prolonged latencies to name the color of “threat” words, such as “panic,” presumably because of enhanced vigilance to them. The second procedure uses the dot-probe test, which measures attention orienting. Reaction time to a spatial probe is quantified as a function of the proximity of the probe to “threat” words or pictures (Bar-Haim, Lamy, & Pergamin, 2007; Mogg & Bradley 1998). Adults with anxiety show faster reaction times to probes proximal to threatening stimuli, an effect attributed to enhanced vigilance to threats. In both procedures, there are relatively subtle but consistent positive associations between adult anxiety and reaction times to threat presentations. Some evidence suggests similar effects in childhood anxiety disorders (Monk, Nelson, McClure et al., 2006; Pine, Mogg, Bradley et al., 2005c). Beyond these two procedures, other less frequently used indices quantify attentional resources during self-monitoring of attention states. In adolescents an association has been reported between aberrant anxiety-state monitoring with anxiety disorders as well as panic disorder in their parents (Pine, Klein, Roberson-Nay et al., 2005b). Finally, diagnostic specificity of cognitive biases is in question, because biases have also been found in depression. In addition, cognitive bias for threat does not appear to be a marker of risk because it occurs primarily in symptomatic adults and disappears with treatment (Williams, Mathews, & MacLeod, 1996). Nevertheless, manipulating bias experimentally has been shown to alter adults’ stress responses (MacLeod, Rutherford, Campbell et al., 2002). Brain Imaging Two imaging procedures have been used in pediatric anxiety disorders, neuromorphometry, which examines brain structure, and functional magnetic resonance imaging (fMRI), which reflects blood flow changes during cognitive processes. Two sets of studies have compared brain structure in pediatric anxiety disorders with healthy comparisons. The first, which examined 10 adolescents with generalized anxiety and healthy comparisons (De Bellis, Casey, Dahl et al., 2000a, 2002), found larger volumes in patients’ amygdala and superior temporal gyrus. The second study involved 15 adolescents with mixed anxiety disorders (Millham, Nugent, Drevets et al., 2005). Consistent with findings in adults, this study found reduced amygdala volume in pediatric anxiety disorders, particularly in generalized anxiety disorder. The difference disappeared after successful treatment. Three fMRI studies report amygdala activity in pediatric anxiety disorders or related states in response to facial photographs. One study found enhanced amygdala activation during the viewing of evocative faceemotion displays (Thomas, Drevets, Dahl et al., 2001). These findings, consistent with those in adults, implicate amygdala hypersensitivity in some forms of anxiety. The second study found no increased amygdala activation in anxious adolescents but observed enhanced activation in the ventral prefrontal cortex, a region implicated in extinction (Monk, Nelson, McClure et al., 2006). Moreover, prefrontal cortex activity correlated negatively with anxiety severity in patients, suggesting that anxiety reflects perturbed functioning in a distributed neural circuit regulated, in part, by the prefrontal cortex. A final study compared amygdala activity in adults classified as inhibited or not inhibited in childhood (Schwartz, Wright, Shin et al., 2003). Enhanced amygdala activity was found in the formerly inhibited individuals, implicating amygdala function in risk for anxiety. Treatment Distress and impairment engendered by anxiety disorders and their long-term liability highlight the need for effective treatments. Some interventions, such as cognitive–behavior therapy (CBT), are based on a theoretical model of anxiety; others, such as selective serotonin reuptake inhibitor (SSRI) medications, follow from demonstrated efficacy in adult anxiety disorders. The literature is replete with case studies reporting efficacy of treatments. The review is of systematic controlled trials. Psychotherapy CBT is the best-studied intervention. Because CBT is based on the notion that distorted cognitions underlie anxiety symptoms, aspects of many CBT treatments focus on the child’s CHAPTER 39 640 9781405145497_4_039.qxd 29/03/2008 02:52 PM Page 640

thought processes, aiming to replace negative beliefs with more realistic neutral cognitions. Some CBT treatments recruit the family’s active involvement to facilitate exposure. The contribution that parents can make in treatment is likely to vary as a function of the child’s disorder and age. A major positive feature of CBT is the availability of treatment manuals. CBT has been compared with no-treatment waitlist controls (Kendall, 1994; Kendall, Flannery-Schroeder, Panichelli-Mindel et al., 1997) or a non-specific control intervention (Beidel, Turner, & Morris, 2000; Last, Hansen, & Franco, 1998; Silverman, Kurtines, Ginsburg et al., 1999). While often used in psychotherapy trials, the use of waitlist controls is methodologically problematic when applied to clinic patients. This disposition confirms to patients that they require treatment but it is withheld. Not only might such an intervention fail to help anxiety, it may have a deleterious impact. The most informative studies are those that have relied on a credible comparison treatment. Finally, it is essential that treatment outcome be evaluated by individuals who are not aware of the treatment delivered, rather than by the therapist. In this fashion, one ensures that biases introduced by treatment allegiances do not influence estimates of outcome. These design features are very infrequently met in current studies of psychotherapy in anxiety disorders. CBT was examined in two systematic studies by Kendall (1994) and Kendall, Flannery-Schroeder, Panichelli-Mindel et al. (1997). Children received CBT for 16 weeks, or were on a waitlist for 8 weeks before then receiving CBT. In both trials, relative to the waitlist, CBT was significantly superior. Moreover, sustained reductions in anxiety continued over several years. Waitlist controls have been used in other studies of CBT; only three studies used “attention” controls (Beidel, Turner, & Morris, 2000; Last, Hansen, & Franco, 1998; Silverman, Kurtines, Ginsburg et al., 1999), with one finding efficacy for CBT in social phobia (Beidel, Turner, & Morris, 2000). Other studies have examined variations in treatment, providing preliminary evidence that either parental involvement (Mendlowitz, Manassis, Bradley et al., 1999) or a group-based format (Barrett, Dadds, & Rapee, 1996) may lead to particularly high rates of response. Finally, on the basis of a systematic trial of group CBT, group family CBT and waitlist control, one study concluded that CBT could be implemented effectively in a group format (Barrett, Duffy, Dadds et al., 2001). While results show that CBT produces significant gains in children with anxiety disorders, considerably more work is needed, particularly with credible control conditions. A recent comparative efficacy study raises major unanticipated questions on the comparative efficacy of CBT, relative to pill-placebo and SSRI medication, in the treatment of adolescent depression (March, Silva, Petrycki et al., 2004). These findings emphasize the need for a comparable largescale CBT/SSRI study in anxiety disorders. Such a study in child anxiety disorders is ongoing. The success of CBT in the treatment of impairing anxiety disorders has raised questions on the role of this treatment for prevention. Attempts to use CBT preventatively have typically relied on what is termed “secondary” prevention, whereby children with mild anxiety receive CBT. While results generally suggest that CBT reduces anxiety symptoms in such groups (Rapee, Kennedy, Ingram et al., 2005), whether results apply to primary prevention is unclear. These interventions have been shown to work in children in the preschool years and onwards. Because children with symptoms are targeted in this work, such interventions might be characterized as therapeutic rather than preventive. Far less work has used alternative approaches, targeting broader portions of the population independently of those with mild symptoms or other risk factors. Pharmacotherapy SSRIs have documented efficacy in virtually all adult anxiety disorders. Four placebo-controlled trials have been published for SSRIs in pediatric anxiety disorders. The first large multisite 8-week study found that fluvoxamine was superior to placebo in children with either social anxiety, separation anxiety or generalized anxiety disorders (RUPP, 2001). Another large study demonstrated comparable benefit for paroxetine over placebo, in children and adolescents with social anxiety disorder (Wagner, Berard, Stein et al., 2004). Finally, two modest-sized studies demonstrated efficacy for fluoxetine and sertraline, each relative to placebo (Birmaher, Axelson, Monk et al., 2003; Rynn, Siqueland, & Rickels, 2001). Concern about SSRIs emerged in 2002–2004, following reports that SSRIs were associated with a two-fold increase in suicidal ideation or behavior, relative to placebo treatment (approximately 4% versus approximately 2%). This observation led to cautionary statements from regulatory officials in Europe and the USA, although debate continues concerning the significance of these data (Vasa, Carlino, & Pine, 2006). Diagnosis did not moderate this association, suggesting that concerns might apply equally to anxiety and mood disorders. A previous literature review (Klein & Pine, 2002) indicated that there was inconsistent support for the efficacy of tricyclic antidepressants in children with separation anxiety. Finally, although there have been some reports on the use of benzodiazepines in anxious children (Klein & Pine, 2002), the efficacy and safety profile of the SSRIs weaken consideration of benzodiazepines. Conclusions Multiple findings have documented the importance of childhood anxiety disorders. These include their elevated prevalence, their associated impairment, the fact that they put children at risk for later depression and their moderate but significant continuity with anxiety disorders in adulthood. Epidemiological studies have generated divergent rates of current anxiety disorders. The evidence suggests 5–10% point prevalence in the general population, with girls over-represented. Some have found greater stability of anxiety in girls than ANXIETY DISORDERS 641 9781405145497_4_039.qxd 29/03/2008 02:52 PM Page 641

boys. Childhood anxiety disorders predict adult anxiety and depression, but no other psychopathology. Knowledge of antecedents would enable identification of children at risk and the development of preventive efforts. Few antecedents have been established. Early inhibited temperament is weakly related to later anxiety, especially social phobia. A modest influence for genetic transmission has been found, with non-shared environmental factors having a greater role. The non-genetic factors in childhood anxiety disorders are poorly understood. As a result, they make little contribution to the clinical management of children with anxiety disorders. Models of brain circuits that regulate fear in animals, also studied in adults, are being applied to children. Early studies suggest that children show abnormalities in underlying fear circuitry, as measured by startle responses to unconditioned fear stimuli, and information processing of fear-related stimuli. However, it is difficult to determine which is cause and which is effect. Neuroimaging studies have focused on the hypothesis of amygdala involvement in anxiety. At this time, the best-documented biological feature of childhood anxiety is respiratory dysregulation, as indexed by hypersensitivity to CO2 exposure in children with separation anxiety disorder. Treatment of anxiety disorders encompasses psychotherapeutic and psychopharmacological interventions. Most treatment studies have included a mixture of anxiety disorders. Most behavioral treatment studies have methodological limitations, but there is evidence of short-term and sustained improvement. SSRIs have been shown to be effective in childhood anxiety disorders. Treatments based on empirical evidence can now be offered to children with anxiety disorders. References Achenbach, T. M. (1991). Manual for the child behavior checklist and 1991 child behavior profile. Burlington, VT: University of Vermont, Department of Psychiatry. 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648 In this chapter we first address the issue of operational definitions of suicidal phenomena in research and clinical practice, followed by consideration of the variety of motives and intentions associated with acts of self-harm in young people. The rates of suicidal behaviors are presented, in conjunction with a summary of research on risk and protective factors. Clinical assessment issues and possible outcomes following an episode of self-harm are described. Treatment options, including psychological interventions and medication, are reviewed, with particular consideration of the issue of engagement in treatment with young people and their families. Finally, we consider factors that influence help-seeking and outline prevention initiatives. Range of Suicidal Behaviors Including Suicide Ideation, Deliberate Self-Harm and Suicide Many young people consider suicide or self-harm at some point in their lives. Some carry out non-suicidal acts of self-injury, while fewer make suicide attempts. A small minority will die, either intentionally or unintentionally. There is a continuum of suicidality but there are also two main points at which discontinuity exists. First, of those who have suicidal ideas only a small proportion engage in some form of deliberate self-harm (DSH). This represents an important behavioral threshold. Second, some people engage in DSH once, never to repeat, while others carry out repeated acts of DSH. Definitions of Terms Suicide ideation is defined as thoughts about an act of DSH or suicide, including wishing to kill oneself, making plans of when, where and how to carry out the act, and having thoughts about the impact of one’s self-harm or suicide on others. DSH is defined as any form of non-fatal selfpoisoning or self-injury (such as cutting, taking an overdose, hanging, self-strangulation and running into traffic), regardless of motivation or the degree of intention to die. Suicide includes deaths resulting directly from acts of deliberate selfharm. Official verdicts in the UK, and many other countries, are determined by the coroner and are classified using ICD10 (World Health Organization, 1996). To reach a verdict of suicide a coroner needs to be satisfied that the act was selfinflicted and that death was the intended outcome. However, strict adherence to these criteria may result in underestimation of the true extent of suicide. Operational definitions are the subject of much debate in both suicide research and clinical practice (Beck, Davis, Frederick et al., 1973; Maris, Berman, Maltsberger et al., 1992; O’Carroll, Berman, Maris et al., 1998). Motives for Suicidal Behaviors and DSH Acts of self-harm may have a variety of motives or intentions, such as finding one’s thoughts or one’s situation unbearable, wanting to die or needing to communicate to others the extent of current distress (Bancroft & Hawton, 1983; Hjelmeland, Stiles, Bille-Brahe et al., 1998). The patterns of motives for DSH described by people who have self-harmed are relatively consistent across the lifespan (Hjelmeland & Groholt, 2005) and across countries (Hjelmeland, Hawton, Nordvik et al., 2002). There are differences according to the method of DSH. In a school-based survey, adolescents who took overdoses often said they wanted to die, whereas those who cut themselves more often reported self-punishment and escape from a terrible state of mind as motives for their DSH (Rodham, Hawton, & Evans, 2004). Escape from a difficult state of mind is a common motive for DSH in adolescents (Hawton, Cole, O’Grady et al., 1982; Kienhorst, de Wilde, Diekstra, & Wolters, 1995). Depression and hopelessness are related to an expressed desire to die as a reason for DSH (Boergers, Spirito, & Donaldson, 1998). Some clinicians and researchers have distinguished selfmutilation as having distinctly different motivations compared with other types of deliberate self-harm. Self-mutilation is defined by Favazza (1992) as the deliberate destruction or alteration of body tissue without conscious suicidal intent, most often by cutting. This behavior is thought to reduce anger, tension or dissociative numbness. This definition suggests habitual cutting among adolescents who lack suicidal intent. However, studies of older individuals who had engaged in self-mutilation behavior indicated a significant risk of subsequent suicide (Stanley, Gameroff, Michalson et al., 2001) and several recent studies have identified high rates of psychiatric morbidity and other risk-taking behaviors among this group of young people (Guertin, Lloyd-Richardson, Spirito et al., 2001; Muehlenkamp & Gutierrez, 2004). On balance it is probably best to consider self-mutilation as part of the continuum of suicidal Suicidal Behavior and Deliberate Self-Harm Keith Hawton and Sarah Fortune 40 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 648 Rutter’s Child and Adolescent Psychiatry, 5th Edition, Edited by M. Rutter, D. V. M. Bishop D. S. Pine, S. Scott, J. Stevenson, E. Taylor and A. Thapar © 2008 Blackwell Publishing Limited. ISBN: 978-1-405-14549-7

phenomena, given that sometimes it can lead on to both suicide attempts and death by suicide. Establishing the intent or motives for an episode of DSH can be complicated as adolescents are often ambivalent about their possible suicidality. In addition, fluctuating mood states can make it difficult to get clear information from adolescents, particularly retrospectively. Self-reported intent may also be influenced by the aftermath of the DSH act. The method of DSH is often taken as a proxy measure of intent. This may be problematic for three reasons. First, young people are known to underestimate risks and habitually engage in behaviors that carry high risk (Millstein & Halpern-Felsher, 2002). Thus, they may not intend to die but nevertheless select a method of DSH that is lethal or, conversely, they do intend to die but select a method that is relatively benign. Second, many young people have poor knowledge about the potential lethality of substances taken in overdose (Harris & Myers, 1997). Third, young people may switch between different methods of deliberate self-harm. Presentation with a relatively low lethality method may follow past acts involving more dangerous methods or may be followed by future episodes in which a more lethal method is used (Fortune, 2006). Introduction to the “Suicidal Process” Among adolescents, suicidal thinking is relatively common in the community, deliberate self-harm is less common and suicide is a rare event (Evans, Hawton, & Rodham, 2005a). To date there has been little research on the extent to which the spectrum of suicidal behaviors may appear or disappear in the lives of young people. Runeson, Beskow, & Waern (1996) have described the “suicidal process,” which they define as an interaction between the individual and their environment that accumulates in such a way that suicidal ideas become plans, and plans are acted upon. They argue that the suicidal process operates at both conscious and unconscious levels. The person’s experience of the process may or may not be communicated to others, but represents increasing vulnerability to acts of DSH and possibly suicide. Broader Developmental Processes The development of suicidal phenomena must be considered in the context of the broader developmental challenges faced by children and adolescents in which emerging physical, cognitive and personality characteristics transform the individual from a child to a young adult. Children pass through a series of stages in intellectual development. Some time after the age of 11 years the child begins to break away from tangible objects towards abstract principles and hypothetical possibilities (Piaget, 1968) and become increasingly able to consider abstract ideas such as the meaning of life. Conceptualizations of death reflect these cognitive changes and start with an early realization, around 8 years of age, that everyone dies (Mishara, 2003), through to an existential “choice to live” during adolescence. Erikson (1968) argued that the key developmental task of adolescence is development of identity versus role confusion, with the peer group assuming primacy over the family as part of this process. The exploration of intimate relationships during this developmental phase makes adolescents particularly vulnerable to rejection. At the same time, the desire to fit in with peers makes adolescents vulnerable to the risk of taking on the behaviors of deviant peers. Youth culture may also have impact on the likelihood of suicide. Adolescents in western cultures appear to be less judgmental about suicide compared with their parents and modern youth culture may portray suicide in positive terms (Cantor, 2000). Youth culture has also de-emphasized the religious–moral dimension of suicide while simultaneously emphasizing an individual’s right to suicide (Bagley & Ramsay, 1997). Population Prevalence of Suicide, Suicidal Ideation and DSH Suicide Reported rates of suicide deaths among children and adolescents around the world vary considerably as can be seen in Table 40.1. Some of this diversity may reflect differences in definition as outlined above, and the cultural and legal mores that surround this issue. Generally, more males than females die by suicide in all countries for which data are published, with the exception of China (Cantor & Neulinger, 2000). In a recent large population-based study in India suicide rates were also found to be higher among adolescent females compared to adolescent males (Aaron, Joseph, Abraham et al., 2004). These findings are the reverse of those in adolescents who have died by suicide in other countries. In several countries rates of suicide are higher in indigenous or aboriginal populations, particularly among young people. For example, First Nations people in the USA (US Department of Health and Human Services, Centers for Disease Control and Prevention, & National Center for Health Statistics, 2004), Metis and Inuit in Canada (Kirmayer, Malus, & Boothroyd, 1996), Australian Aborigines (Tatz, 2001) and New Zealand Ma¯ori (Ministry of Health, 2005). Historically, the rate of suicide among Black people in the USA has been considerably lower than White people (Bingham, Bennion, Openshaw et al., 1994); however, from 1980 to 1995 there was a dramatic increase in suicide deaths among Black youth ( Joe & Kaplan, 2001). Youth suicide rates in the UK are declining following a period in which rates in young males had been rising alarmingly. It should be noted that official statistics markedly underestimate the true rates of suicide, especially in children and adolescents, with some apparent suicide deaths being recorded as open verdicts, accidents or misadventure (Madge & Harvey, 1999). In the UK, the rate of suicide and undetermined deaths for adolescent males 15–19 years old in 2003 was 6.58 per 100,000 and 2.24 per 100,000 for females of the same age. The rate of suicide and undetermined deaths among children aged 10–14 years was much lower, at 0.62 per 100,000 for males and 0.42 per 100,000 for females (Office of National Statistics, 2004). SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 649 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 649

CHAPTER 40 650 Suicidal Ideation and DSH A recent systematic review on the prevalence of suicidal phenomena in adolescents based on community or school-based studies in several countries demonstrated that suicidal ideation is more common than DSH, which is in turn more common than attempted suicide. Nearly 1 in 5 adolescents had thought about suicide in the previous year. The mean lifetime prevalence of deliberate self-harm was 13%, with 26% reporting deliberate self-harm in the previous year. The mean proportion of adolescents who had attempted suicide was 10%, with 6% making a suicide attempt in the previous 12 months. Rates of suicidal phenomena were higher among females than males (Evans, Hawton, Rodham et al., 2005b). In the UK, relatively few studies have been conducted on the prevalence of suicidal ideation and self-harm in the community. In a school-based study of 6020 students, 15% reported thoughts of deliberate self-harm (which had not been acted on) in the preceding year. This was much more common among females (22%) than males (9%). DSH in the past year occurred in 7% and was also much more frequent among females (11%) than males (3%; Hawton, Rodham, Evans et al., 2002a). In contrast, in a large national study of suicidal phenomena among children and adolescents 5–15 years old, based on parental report, 1% of 5- to 10-year-olds had ever tried to harm, hurt or kill themselves, rising to 2% among those aged 11–15 years (Meltzer, Harrington, Goodman et al., 2001). Parents are often unaware of DSH acts by their offspring (Huey, Henggeler, Rowland et al., 2004; Meltzer, Harrington, Goodman et al., 2001; Sourander, Aromaa, Pihlakoski et al., 2006), especially where self-cutting is involved. Two studies that used a similar methodology to Hawton, Rodham, Evans et al. (2002a) were conducted in Australia (De Leo & Heller, 2004) and Norway (Ystgaard, Reinholdt, Husby et al., 2003); these suggested that rates of DSH in adolescents in the UK, Australia and Norway are similar. In a comparative study, again using equivalent methodology, rates of DSH were also similar in Belgium, but considerably lower in the Netherlands (Hawton, Rodham, & Evans, 2006). There appear to be some differences between rates of nonfatal suicidal behavior in children and adolescents of different ethnic groups. In the USA, for example, several studies have indicated that Hispanic youth, particularly females, experience higher rates of suicide ideation, DSH and hopelessness than their White and Black peers (for review see Canino & Roberts, 2001). In New Zealand, a large national health study found that Ma¯ori youth reported significantly higher rates of depression, suicide ideation and suicide attempts in the last year than European/Pakeha students (Adolescent Health Research Group, 2005). There have been a small number of studies of DSH among ethnic minority children and adolescents in the UK which have produced somewhat conflicting results. The most robust data come from the school-based study described above, in which DSH was less common among Asian (7%) and Black (7%) Male age-specific Female age-specific rate per 100,000 rate per 100,000 population population Country Year 5–14 years 15–24 years 5–14 years 15–24 years Australia 2002 0.3 17.9 0.3 4.4 Austria 2004 0.4 21.6 0.0 4.3 Belgium 1997 1.0 19.2 0.0 5.4 Canada 2002 0.9 17.5 0.9 5.2 China 1999 0.9 5.4 0.8 8.6 Denmark 2001 0.6 12.5 0.0 2.4 Finland 2004 1.2 33.1 0.3 9.7 France 2002 0.6 11.9 0.4 3.1 Germany 2004 0.4 10.5 0.2 2.7 Ireland 2002 0.4 27.3 0.7 4.4 Italy 2002 0.2 6.5 0.2 1.5 Japan 2003 0.5 15.5 0.6 7.8 Lithuania 2004 2.7 42.9 0.5 7.4 Netherlands 2004 0.7 7.3 0.2 2.6 New Zealand 2002 0.0 22.8 0.0 11.0 Norway 2003 1.9 20.6 1.0 6.3 Russian Federation 2004 3.6 47.4 1.0 8.2 Spain 2003 0.1 6.8 0.1 2.1 Sweden 2002 0.7 14.6 0.5 4.5 UK 2002 0.1 8.2 0.1 2.4 USA 2002 0.9 16.5 0.3 2.9 Table 40.1 Male and female suicide rates for children, adolescents and young adults for selected countries (World Health Organization, 2006). Note: Comparison years vary by country because of availability of data. 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 650

girls than White girls (12%). Rates of DSH were similar among Asian and White males (3%; Hawton, Rodham, Evans et al., 2002a). More recent studies have reported similar (Bhugra, Thompson, Singh et al., 2003) or lower rates of DSH among Asian youth (Bhugra, Thompson, Singh et al., 2004). This issue is reviewed in Bhugra and Bhui (2007). Methods of Suicide and DSH by Gender and International Differences There is significant variation among cultures in the methods most commonly used for suicide. The preferred methods of suicide in any given country may have an impact on suicide rates, given that some methods are potentially more lethal than others. In addition, deaths involving a certain method may increase or decrease depending on the availability of that method (Grossman & Kruesi, 2000; Hawton, 2005). For example, in the USA firearms are the most common method of suicide among both Black and White young people, but account for a relatively small number of deaths in the UK, New Zealand and Australia. The substitution of method relies on both the acceptability and availability of alternative methods; the increasing rate of hanging in young people suggests that it has become an increasingly acceptable method of suicide (Centers for Disease Control, 2004). It is also extremely accessible as well as having a high rate of lethality. The reason for the spread in acceptability of hanging as a method of suicide is not known. The globalization of information has already resulted in rapid transmission of previously unknown and very lethal methods of suicide; for example, the spread of the use of charcoal burning from Hong Kong to Taiwan and Japan and the rapid rise in the popularity of this method. The mechanisms underlying the apparent increased acceptability, cultural meaning and preference for methods of suicide such as this require further research, including the likely role of the media, including the Internet, in influencing this trend. In India, in contrast with other countries, hanging is a slightly more frequent method of suicide in girls (57%) than boys (50%), whereas poisoning is slightly more common in boys (50%) than girls (37%; Lalwani, Sharma, Kabra et al., 2004). The use of toxic pesticides in agrarian communities such as in China, India (Prasad, Abraham, Minz et al., 2006) and Sri Lanka (Eddleston, Gunnell, Karunaratne et al., 2005b) means that a similar method (self-poisoning) is associated with much higher mortality in these countries than in countries where analgesics and other medications are the most frequently used substances for self-poisoning. The medical management of organophosphate poisoning is difficult and a lack of adequate medical services and distances to hospitals in developing countries may elevate death rates (Eddleston, Eyer, Worek et al., 2005a). At the community level the most common methods of DSH in the UK and many other countries are cutting and overdose. Hawton, Rodham, Evans et al. (2002a) found that cutting (65%) and overdose (31%) were the main methods of DSH among adolescents in the community. Studies using the same methodology showed similar rates of cutting in Australia (59%; De Leo & Heller, 2004) but higher rates in Norway (74%; Ystgaard, Reinholdt, Husby et al., 2003). However, only a minority of young people engaging in DSH in the community go to hospital, with those taking overdoses most likely to do so (Hawton, Rodham, Evans et al., 2002a). In studies based on presentations to general hospitals in the UK, the majority of adolescents had harmed themselves by taking an overdose, self-poisoning with analgesics being particularly common (Hawton, Hall, Simkin et al., 2003). Risk Factors Associated with Suicidal Phenomena in Children and Adolescents An overall model of suicide behavior can help the clinician or researcher conceptualize the main contributory factors identified in a wide range of research studies. This can also provide a framework to support formulations and treatment planning. In such a model (Beautrais, 2000) suicidal behaviors are viewed as the endpoint of adverse life events in which multiple risk factors combine to encourage the development of suicidal behaviors (Fig. 40.1). This essentially represents a stress–diathesis model (Schotte & Clum, 1982), which suggests that temperamental and genetic factors and early experiences may make some young people particularly vulnerable to subsequent internal or external stressors. There are a number of comprehensive reviews of the research literature on risk factors associated with fatal and nonfatal suicide behaviors among children and adolescents to which the reader is directed (Beautrais, 2000; Brent, 1995; Bridge, Goldstein, & Brent, 2006; Evans, Hawton, & Rodham, 2004; Gould, Greenberg, Velting et al., 2003). Below we highlight contributory factors for which there is at least reasonably strong evidence. Genetic and Neurobiological Aspects of Suicidal Behavior in Young People Suicidal behavior runs in families (Brent, Bridge, Johnson et al., 1996a). However, the risk in these families is not entirely accounted for by the increased rates of psychiatric disorder. The heritability of impulsive aggression also appears to be important (for a review see Brent & Mann, 2005). Twin studies have shown that the concordance for fatal and non-fatal suicidal behavior is higher among monozygotic than dyzygotic twins (Roy, 1993). The clustering of suicidal behavior in families cannot be explained entirely by behavioral imitation (Brent & Mann, 2005). Importantly, adoption studies have shown elevated rates of suicide among the biological relatives of adoptees who die by suicide compared with those of nonsuicidal adoptees (Roy, Rylander, & Sarchiapone, 1997). Genetic factors may affect the risk of suicide behaviors by their influence on neurobiology and much of this work SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 651 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 651

CHAPTER 40 652 has arisen from the investigation of genetic factors in depression (for review see Levinson, 2006). The relationship between genetics and depression is dealt with in more detail in chapter 37. Deviations in the serotonin system are one of the most robust neurobiological findings associated with suicidal behavior (Asberg & Forslund, 2000). The relationship between serotonin dysregulation and suicide behavior may reflect poor impulse control, which is observed in suicidal, violent and impulsive behaviors. Earlier studies examined serotonin metabolites in cerebrospinal fluid and found lower than average levels of 5-hydroxytryptamine (serotonin 5-HT) and the metabolite 5-hydoxyindoleacetic acid (5-HIAA) in suicide victims (Arango, Underwood, Gubbi et al., 1995), and people at risk of repetition of suicide attempts and suicide (Nordstrom, Samuelsson, Asberg et al., 1994). More sophisticated neuroanatomical studies have identified a reduced density of serotonin 1A receptors and serotonin transporter receptors in the prefrontal cortex and brainstem of those who have died by suicide (Arango, Underwood, Boldrini et al., 2001; Mann, Huang, Underwood et al., 2000). Dysregulation of serotonin function may predispose a person experiencing stressful events to react impulsively (Mann, Brent, & Arango, 2001). There is less evidence for other neurobiological markers for suicidal behaviors such as dopamine, noradrenaline, cortisol and serum cholesterol (Asberg & Forslund, 2000; Bondy, Buettner, & Zill, 2006). The main focus of interest in the genetic studies of suicidal behavior has been on three gene types: trytophan hydroxylase (TPH), serotonin transporter (SERT), located on chromosome 17, and serotonin A receptor genes (Arango, Underwood, Boldrini et al., 2001). Serotonin transporter polymorphisms, particularly the “short” allele of the 5HTTLPR genotype, are associated with suicidal behavior in adults with psychiatric disorder and in particular violent attempts (Lin & Tsai, 2004). More recent studies in adults have explored the role of cannabinoids in the model of anxiety and stress responses underpinning suicidal behavior, in particular cannabinoid receptors (CB1), corticotropin-releasing hormone (CRH) and γ-aminobutyric acid (GABA) (Bondy, Buettner, & Zill, 2006). Despite the interest in this area to date, there are relatively few replicated findings or meta-analyses, particularly in children and adolescents. Psychological and Cognitive Characteristics Psychological characteristics associated with suicidal behavior include hopelessness (Evans, Hawton, & Rodham, 2004), dichotomous (all or nothing) thinking, negative biases in future judgment (Pfeffer, 2000; Williams & Pollock, 2000) and an external locus of control, or the belief that “things happen to you” because of forces outside your own control (Kienhorst, de Wilde, Diekstra et al., 1992). Impaired problem-solving may be another contributory factor (Speckens & Hawton, 2005). This appears to be related to overgeneralized autobiographical memory (Williams & Pollock, 2000), although this phenomenon is not specific to suicidal behavior (Evans, Hawton, & Rodham, 2004). Fig. 40.1 Conceptual model of domains of risk factors for suicide and attempted suicide. SES, socio-economic status (After Beautrais, 2000, p. 429, with permission from the publisher.) Genetic and biological factors Social and demographic factors Age, gender, ethnicity, SES Environmental factors Life events, contagion, media, access to methods Suicide attempt and suicide Psychiatric morbidity Mental disorders, personality disorders, comorbidity, previous attempts, previous psychiatric care Family characteristics and childhood experiences Parental phychopathology, parental care, abuse, family dysfunction Personality traits and cognitive styles 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 652

Certain personality characteristics such as impulsivity, aggression, neuroticism and trait anxiety may act as intermediate factors that are relatively independent from major psychiatric disorders (Bridge, Goldstein, & Brent, 2006). Irritability and impulsivity have also been strongly associated with suicide in young men (Conner, Meldrum, Wieczorek et al., 2004) and non-fatal acts in both genders (Bridge, Goldstein, & Brent, 2006). Aggression is also associated with DSH (Sourander, Aromaa, Pihlakoski et al., 2006). A review of the associations between attention deficit/hyperactivity disorder (ADHD) and suicidal behavior concluded that they are modest, with elevated risk for fatal and non-fatal suicidal behavior, particularly in males, mediated by comorbid conditions, notably depression, conduct disorder and substance abuse, with the risk considerably elevated in young people with all three conditions (James, Lai, & Dahl, 2004). Psychiatric Disorders Associated with DSH and Suicide Many studies have demonstrated high rates of mental illness in adolescents engaging in both fatal and non-fatal suicidal behavior (for review see Evans, Hawton, & Rodham, 2004). In this section we highlight strong and recent findings about the relationship between mental illness and suicidal phenomena which have been investigated prospectively through longitudinal studies, retrospectively through psychological autopsy studies, and smaller cross-sectional and clinical population studies (which often provide less robust findings). Although mental illness is present in many children and adolescents who engage in suicidal behaviors, clearly not all people who experience mental illness engage in suicidal behavior, so it may be a strong precursor but not a complete explanation. In a systematic review of psychological autopsy studies (Cavanagh, Carson, Sharpe et al., 2003, p. 400) results of seven studies of adolescents or young adults suggested that 47–74% of suicides examined were attributable to a mental disorder, of which affective disorders made the greatest contribution. This review also highlighted that comorbidity, particularly comorbidity of mental disorder and substance abuse, made a strong contribution to the risk of suicide. An earlier review (Marttunen, Aro, & Lonnqvist, 1993) indicated that antisocial behavior was present in 43–73% of suicide deaths in adolescents, often in combination with depressive symptoms and/or substance abuse. Several more recent psychological autopsy studies (Fortune, Stewart, Yadav et al., 2007; Houston, Hawton, & Sheppard, 2001; Portzky, Audenaert, & van Heeringen, 2005) point towards an interaction among mental illness, substance abuse and interpersonal problems (and, for some, antisocial behaviors). In a case–control study of young people who had died by suicide, serious suicide attempters and a non-suicidal control group, the same risk factors of mood disorder, requirement for psychiatric care, educational disadvantage and stressful life events were associated with both death by suicide and serious attempts, although the relative weighting of the factors was different. Mood disorders had a higher odds ratio for attempts than for death by suicide, and stressful life events had a higher odds ratio for suicide than attempts (Beautrais, 2003). However, it must also be borne in mind that 5–10% of young people who die by suicide have no mental health disorder. This group tend to include those with less disturbed families, who have no previous history of suicide behavior (Marttunen, Henriksson, Isometsae et al., 1998). Multiple co-occuring mental disorders are common among children and adolescents presenting with suicidal behaviors and those who have died by suicide. There is evidence to suggest that a greater number of diagnoses is associated with worse psychosocial outcomes generally, and more specifically risk of DSH (Beautrais, Joyce, Mulder et al., 1996b; Fergusson & Lynskey, 1996; Miller & Taylor, 2005; Sansone, Gaither, Songer et al., 2005) and suicide (Brent, Baugher, Bridge et al., 1999; Reith, Whyte, Carter et al., 2004). Mood Disorders Depression is the most prevalent mental health disorder reported in psychological autopsy studies (Brent, Baugher, Bridge et al., 1999; Houston, Hawton, & Sheppard, 2001; Portzky, Audenaert, & van Heeringen, 2005; Shaffer, Gould, Fisher et al., 1996) and non-fatal suicidal behaviors (Evans, Hawton, & Rodham, 2004). Hopelessness is an important mediating variable between depression and suicidal behavior (Thompson, Mazza, Herting et al., 2005). There is also a link between suicide ideation and depression, with increasing severity of depression associated with increasing likelihood of suicide ideation (Allison, Roeger, Martin et al., 2001). The course of depression across adolescence also appears to influence suicidality. In a longitudinal study of 193 children and adolescents, persistent depression was associated with significantly higher rates of suicidal ideation and suicide attempts. Depressed females were more likely to experience recurrent episodes, while males tended to experience persistent mental illness (Dunn & Goodyer, 2006). Whereas most studies have concerned adolescents with an overt mood disorder, in a recent longitudinal study of 10- to 17-year-olds from a birth cohort, those presenting with subthreshold mood disorders (i.e., those with some symptoms but not meeting the criteria for a diagnosis) had an increased risk of later development of depression, anxiety, suicidal ideation and DSH. The risk, in terms of suicide ideation, associated with subthreshold depression was similar to that of major depressive disorder (Fergusson, Horwood, Ridder et al., 2005). Bipolar disorder has also been associated with elevated rates of suicide attempts, with the lifetime prevalence ranging from 20% (Strober, Schmidtlackner, Freeman et al., 1995) to 44% (Lewinsohn, Seeley, & Klein, 2003). Case–control studies suggest that bipolar disorder in young people is associated with elevated risk of suicide (Brent, Perper, & Moritz, 1993). Anxiety Anxiety, particularly when comorbid with depression, has SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 653 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 653

been identified as increasing the risk of fatal and non-fatal acts, although this does not appear to be a direct association (Bridge, Goldstein, & Brent, 2006; Evans, Hawton, & Rodham, 2004). In a case–control study anxiety was more strongly associated with suicide attempts than suicide deaths (Beautrais, 2001). Panic attacks have been associated with increased risk of suicidal ideation and DSH (Gould, King, Greenwald et al., 1998). Young adult females who reported multiple suicide attempts had higher rates of childhood anxiety disorders than ideators and those who had made a single suicide attempt (Rudd, Joiner, & Rumzek, 2004). Substance Abuse Substance abuse disorders, including cigarette smoking, are associated with increased risk of suicide attempts (Evans, Hawton, & Rodham, 2004) and suicide deaths (Beautrais, 2000). Several reviews (Esposito-Smythers & Spirito, 2004; Gould, King, Greenwald et al., 1998; Gould, Greenberg, Velting et al., 2003) have shown that substance abuse is more strongly correlated with suicide attempts than ideation and that the relationship is likely to be direct (Evans, Hawton, & Rodham, 2004). Suicide risk is highest among young men and older adolescents with substance abuse (Bridge, Goldstein, & Brent, 2006). Clinically, it can be difficult to establish if substance abuse precedes or follows the mental health difficulties and suicidal phenomena. Up to one-third of young people presenting to hospital following an episode of deliberate self-harm have consumed alcohol around the time of the act (Hawton, Hall, Simkin et al., 2003), and alcohol abuse is associated with increased rates of repetition (Vajda & Steinbeck, 2000). Psychosis Approximately 5% of patients of all ages diagnosed with schizophrenia die by suicide, with young people and those early in the course of illness being most likely to kill themselves (Palmer, Pankratz, & Bostwick, 2005). However, psychotic disorders make a relatively small contribution to the overall youth suicide rate (Beautrais, 2000). Suicide risk is increased among young people with psychotic disorders where there were higher levels of premorbid functioning, better insight, higher intelligence and preservation of cognitive function (Apter & Freudenstein, 2000; Pompili, Mancinelli, Girardi et al., 2004). A recent systematic review of risk factors for suicide among those with schizophrenia identified depression, previous suicide attempts, drug abuse, agitation, fear of mental disintegration, poor engagement with treatment and recent loss as important, whereas specific psychotic symptoms had less predictive value than the factors associated with general psychosocial functioning and affective disturbance (Hawton, Sutton, Haw et al., 2005). Many adolescents with schizophrenia also abuse drugs and alcohol, thus exacerbating the risk for DSH and death by suicide (Apter & Freudenstein, 2000). Conduct Disorder/Antisocial Behavior Antisocial behavior is a risk factor for DSH among females although, perhaps surprisingly, the relationship is less clear for males (Evans, Hawton, & Rodham, 2004). Many of the risk factors for conduct disorder are also risk factors for DSH, including family disruption, childhood abuse, personal and familial substance abuse and negative life events (Apter & Freudenstein, 2000). There are higher than average rates of DSH (Coffey, Wolfe, Lovett et al., 2004; Morgan & Hawton, 2004) and suicide among imprisoned youth (Coffey, Wolfe, Lovett et al., 2004; Shaw, Baker, Hunt et al., 2004). Antisocial behaviors are prominent among young men who die by suicide (Gould, Greenberg, Velting et al., 2003; Marttunen, Aro, & Lonnqvist, 1993) and those with comorbid antisocial and substance abuse disorders (Bridge, Goldstein, & Brent, 2006). Eating Disorders Poor body image and disordered eating are associated with suicidal phenomena and some consider starvation to be a form of suicidal behavior that obviates the need for other methods of DSH. Suicide risk in anorexia nervosa has been estimated to be 2–15% and 0.4–2% for bulimia nervosa, with higher rates among adolescent males than females with eating disorders (Dancyger & Fornari, 2005). Poor Physical Health Related to Psychological Problems The relationship between physical illness and suicide in young people has received less attention than in adult populations. However, psychosomatic and physical presentations among suicidal children and adolescents are important for two reasons. First, although some adolescents with depression may present with similar symptoms to adults, they also commonly present with psychosomatic complaints such as headaches, loss of energy, chest pain, abdominal pain or other physical symptoms (McPherson, 2005). Second, poor physical health and many chronic illnesses are associated with increased risk for suicide ideation (Suris, Parera, & Puig, 1996) and DSH (Evans, Hawton, & Rodham, 2005a), independent of psychiatric disorder (Goodwin, Marusic, & Hoven, 2003; Vajda & Steinbeck, 2000). Environmental Factors Including Biopsychosocial Stressors Family Factors Including Parental Psychiatric Disorders, Violence, Abuse Longitudinal community studies have shown that difficulties in parent–child relationships, including those related to early attachment problems, perceived low levels of parental caring and communication are related to increased risk of suicide and suicide attempts among children and adolescents (Ackard, Neumark-Sztainer, Story et al., 2006; Fergusson & Lynskey, 1995b; Fergusson, Woodward, & Horwood, 2000); similar observations have been made in clinical samples (Lessard & Moretti, 1998; Pfeffer, 2000). CHAPTER 40 654 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 654

Several reviews have concluded that adolescents from families that have experienced parental separation or divorce are at increased risk of suicide behavior, particularly among females (e.g., Beautrais, 2000; Brent, Perper, Moritz et al., 1994a; Gould, Fisher, Parides et al., 1996). It seems that conflict between parents, both before and after their relationship ends, has a detrimental impact on children. Family History of Suicide Behavior Research consistently indicates that a family history of suicidal behavior is associated with increased risk for suicide deaths (Agerbo, Nordentoft, & Mortensen, 2002; Brent, Perper, Moritz et al., 1994a; Brent, Perper, Goldstein et al., 1988; Gould, Fisher, Parides et al., 1996) and non-fatal DSH behavior by adolescents (Hawton, Rodham, Evans et al., 2002a; Johnson, Brent, Bridge et al., 1998; Roy, Rylander, & Sarchiapone, 1997). Similarly, exposure to fatal and non-fatal suicidal behavior in the family increases suicidal ideation in adolescents (Cerel & Roberts, 2005) and has been associated with more violent suicide attempts (Bridge, Goldstein, & Brent, 2006; Roy, Rylander, & Sarchiapone, 1997). Having a suicidal family member may model to adolescents that suicide is a possible solution to overwhelming psychological pain (Roy, Rylander, & Sarchiapone, 1997), although the detrimental effects of living with a parent who has undiagnosed or undertreated mental health problems are also significant (Agerbo, Nordentoft, & Mortensen, 2002). More work is required to clarify the extent to which suicidal behavior can be considered as a construct that is transmitted through families independently of the established association with familial risk of depression, impulsivity and other psychopathology (Brent & Mann, 2005). Parental Mental Health Disorders Parental mental health disorders are associated with increased risk of their children dying by suicide, particularly parental depression and substance abuse (Brent, Perper, Moritz et al., 1994a). Several authors have found an association between poor parental mental health and both suicide ideation and nonfatal suicide behavior (Fergusson & Lynskey, 1995a; Meltzer, Harrington, Goodman et al., 2001; Sourander, Aromaa, Pihlakoski et al., 2006). Childhood Physical and Sexual Abuse A strong and direct association exists between suicide attempts and both childhood sexual abuse and physical abuse (Beautrais, 2000; Evans, Hawton, & Rodham, 2005a). Parental history of childhood sexual abuse is also associated with an increased risk of suicide attempts among offspring (Brent, Oquendo, Birmaher et al., 2002). Bullying is associated with poor mental health, suicide ideation and attempts (Coggan, Bennett, Hooper et al., 2003; Kaltiala-Heino, Rimpela, Marttunen et al., 1999; Sourander, Aromaa, Pihlakoski et al., 2006). There has been recent concern about suicides by young people allegedly bullied by peers using mobile telephones and via the Internet (Smith, 2004). SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 655 Peers, Including the Influence of Peer Suicidal Behaviors and Suicide Clusters The importance of peer relationships and suicidal behaviors among groups of friends is becoming increasingly apparent. Having a friend who attempted suicide in the previous year increased rates of suicide ideation and attempts among both girls and boys (Evans, Hawton, & Rodham, 2004). The relative risk of suicide among those exposed to an index suicide has been shown to be 2–4 times higher in 15- to 19-year-olds, with contagion less salient among those aged over 25 years (Gould, Greenberg, Velting et al., 2003). In a large study in the USA, socially isolated girls were more likely to experience suicide ideation and both boys and girls with dense social networks were less likely to attempt suicide (Bearman & Moody, 2004). Clusters of suicidal acts in adolescents sometimes occur, particularly in institutional settings such as schools and inpatient psychiatric units. This may reflect modeling of the behavior and exposure to similar stressors (Gould, Wallenstein, & Davidson, 1989). Suicide clusters are relatively unusual and account for only 5% of all youth suicides. Subsequent suicide behavior is more likely among young people who were already experiencing mental health difficulties (Beautrais, 2000). Sexual Orientation Gay, lesbian and bisexual young people are at increased risk of engaging in DSH (Remafedi, French, Story et al., 1998; Russell & Joyner, 2001), with estimates of risk ranging 2–6 times that of heterosexual young people (Gould, Greenberg, Velting et al., 2003). In one of the relatively few studies in this area, 59% of males in New York who had made a suicide attempt reported it was related to their sexual orientation and 38% of females who had made an attempt attributed this to issues relating to their sexuality (D’Augeli, Grossman, Salter et al., 2005). No study has yet documented increased rates of death by suicide related to sexual orientation (Gould, Greenberg, Velting et al., 2003). However, gay, lesbian and bisexual youth are more likely to experience risk factors associated with suicide (Shaffer & Pfeffer, 2001), particularly mental health difficulties (Fergusson, Horwood, & Beautrais, 1999). School Several reviews of studies of young suicide attempters (Beautrais, Joyce, & Mulder, 1996a; Evans, Hawton, & Rodham, 2004) and those who die by suicide (Gould, Fisher, Parides et al., 1996) have indicated that more have had school-based difficulties and/or have dropped out of school than have non-suicidal adolescents. Dropping out of school has been shown to be a risk factor for medically serious suicide attempts, in addition to the socio-economic disadvantages that are associated with having few educational qualifications (Donald, Dower, Correa-Velez et al., 2006). Children and adolescents who remain in school but have special educational needs appear to have higher rates of suicidal phenomena than their 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 655

peers without such needs (Denny, Clark, & Watson, 2003; Meltzer, Harrington, Goodman et al., 2001). Proximal Risk Factors/Life Stressors Both psychological autopsy (Marttunen, Aro, & Lonnqvist, 1993) and case–controlled studies (Beautrais, 2000) suggest that, compared with controls, young people who die by suicide experience higher rates of exposure to recent stressful life events such as rejection, conflict or loss following the breakup of a relationship (Brent, Moritz, & Liotus, 1996d; Donald, Dower, Correa-Velez et al., 2006), disciplinary or legal crises (Marttunen, Henriksson, Isometsae et al., 1998). Life stressors are also associated with DSH (Hawton, Hall, Simkin et al., 2003). The nature of the stressors seems to vary according to age. For example, children and younger adolescents describe familial stress, whereas older adolescents typically describe peer-related stressors (Gould, Greenberg, Velting et al., 2003; Hawton, Hall, Simkin et al., 2003). Becoming intoxicated is a short-term solution that many adolescents engage in following crises. Intoxication leads to impaired judgment and decreased inhibition, and can facilitate suicidal behavior (Apter & Freudenstein, 2000). Refugees and asylum seekers face particular psychosocial stressors that are likely to have an impact on young people and their families. Unemployment, social isolation and the difficulties involved in applying for asylum experienced by parents are factors that, together with the high rates of depression, anxiety and post-traumatic stress disorder (PTSD) in this population, may lead to suicidal behavior (Fazel, Wheeler, & Danesh, 2005; Keller, Rosenfeld, Trinh-Shevrin et al., 2003; Sultan & O’Sullivan, 2001). Exposure to Suicide in the Media, Music and the Internet The accumulated evidence suggests that certain types of media reports and portrayals of suicide and attempted suicide can increase the risk of suicidal behavior (for reviews see Hawton & Williams, 2005; Pirkis & Blood, 2001; Pirkis, Francis, Blood et al., 2002; Schmidtke & Schaller, 2000). The greatest influence is probably on methods used for suicide and deliberate self-harm and seems to be particularly marked in young people (Phillips & Carstensen, 1988; Stack, 1991). It appears that such effects are more likely where media reporting or portrayal is dramatic, features details of a specific method of suicide, is on television and is repeated (Pirkis & Blood, 2001; Pirkis, Burgess, Francis et al., 2006b; Stack, 2003). Many children appear to learn about suicide from television (Mishara, 1999; Pirkis & Blood, 2001). Some people may respond quickly to media presentations of suicide, acting impulsively or putting previous thoughts about suicide into action, while others may make a more considered response (Schmidtke & Häfner, 1988). Thus, in addition to potential immediate changes in suicidal behavior, media influences may also have longer-term effects, by changing attitudes, providing information about methods of suicidal behavior or planting the idea that suicide is an appropriate response to problems. While concern has been raised about the possible influence of music (especially certain types of popular music) on suicidal phenomena among children and adolescents, this has received very limited attention in the research literature (Martin, Clarke, & Pearce, 1993). Recently, concern has been raised about Internet sites dealing with suicide and their potential negative influence on adolescent suicidal behavior (Gould, Munfakh, Lubell et al., 2002). The provision of interactive experiences and the development of “online communities” mean that the Internet may have a unique role in influencing suicidal behavior and/or providing peer support and possibly helping prevent suicidal behavior. It is not known if technology-based communication has implications for the consideration of contagion in young people, or what role cyber-bullying (i.e., bullying via Internet, email and text messaging) is a stressor among young people who engage in suicide behaviors. Few studies have been conducted in this area. In a large community study, depressed young people, especially boys, were heavier users of the Internet, more likely to access the Internet at school and more likely to use chat-rooms and interact with peers they saw infrequently in person, and also strangers (Ybarra, Alexander, & Mitchell, 2005). A study of online postings to message boards focusing on self-injurious behavior by young people aged 12–20 years suggested that online interactions provide important social support to users, but that these interactions may also normalize or encourage self-injurious behavior (Whitlock, Powers, & Eckenrode, 2006). The Internet may also provide opportunities for suicide prevention. For example, 6 months after a school-based presentation promoting the use of a website for young people experiencing emotional difficulties, 45% of students said they had visited the website (Nicholas, Oliver, Lee et al., 2004). Availability of Means for DSH/Suicide The preferred method of DSH has an impact on suicide rates, given that some methods are potentially more lethal than others. In the UK, self-laceration and overdose are the most commonly used methods of DSH among children and adolescents (Hawton, Rodham, & Evans, 2006). Children and adolescents who die by suicide in the UK are most likely to have used hanging, self-poisoning, carbon monoxide poisoning or drowning (Hawton, Houston, & Sheppard, 1999a). Deaths involving a certain method may increase or decrease depending on the availability of that method (Grossman & Kruesi, 2000; Hawton, 2005). For example, in the USA firearms are the most common method of suicide (Stack & Wasserman, 2005), but account for a relatively small number of deaths in the UK, New Zealand and Australia. The substitution of one method for another relies on both the acceptability and availability of alternative methods. For example, a decrease in the use of firearms and self-poisoning among young people in the USA was accompanied by an increase in deaths by suffocation, mostly hanging (Centers for Disease Control, 2004). Rates of hanging have also increased among CHAPTER 40 656 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 656

SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 657 young people of both genders in the UK (Gunnell, Bennewith, Hawton et al., 2005). The increasing rate of hanging suggests that this has become an increasingly acceptable method of suicide (Centers for Disease Control, 2004). Hanging is also extremely accessible as well as having a high rate of lethality. The reasons for the spread in acceptability of hanging and the increased use of this method among young females as a method of suicide are not known. The ready availability of pesticides in agrarian communities such as in China and Sri Lanka is associated with the use of these for self-poisoning. Because of their high lethality, suicide rates in young people are relatively high compared with those in developed countries (Eddleston, Gunnell, Karunaratne et al., 2005b). Protective Factors Compared with the volume of research on risk factors, relatively little work has been conducted on factors that protect against the development of suicide behavior in adolescents. The concepts of adversity and resilience are dealt with in chapters 25 and 26. In summary, factors that protect against mental illness associated with suicidal phenomena include good social skills, problem-solving abilities and an internal locus of control (Merry, McDowell, Hetrick et al., 2002). Factors thought to protect against the risk of suicide include enjoyment and involvement with school (Dexheimer Pharris, Resnick, & Blum, 1997), playing sports (Tomori & Zalar, 2000), family cohesiveness (Rubenstein, Halton, Kasten et al., 1998), religious affiliation and a commitment to life-affirming beliefs (Neeleman, Halpern, Leon et al., 1997; Stack, 2000). Impact of Suicide on Peers, School and Relatives Suicide by a peer has a significant impact on their friends, family, school and community. In a series of studies on peers of children and adolescents who died by suicide, Brent, Perper, Moritz et al. (1994b) found worsening of depression among those who were already depressed at the time of their peer’s death and elevated overall rates of depression (Brent, Perper, Moritz et al., 1992), anxiety and PTSD, particularly in the first 6 months after the death (Brent, Moritz, Bridge et al., 1996b). The siblings and parents of adolescents who died by suicide showed elevated levels of grief over a prolonged period of time, with an increased risk of recurrence of maternal depression (Brent, Moritz, Bridge et al., 1996a). Traumatic grief reactions, distinct from depression or PTSD, have also been identified in friends (Melhem, Day, Shear et al., 2004a,b). A small group of adolescents who have lost a peer by suicide may witness the effects of the suicide on the community and “may find themselves wishing that they too could create the same effects” (Rivers, 1995, p. 15). This issue is a particular challenge for postvention among school peers. However, as noted earlier, clusters of suicides do occur in adolescents, they are relatively unusual (Beautrais, 2000). There has been little research into the effects of DSH on parents. In the USA, Wagner, Aiken, Mullaley et al. (2000) showed that parental reactions to suicidal behavior may include anger, fear, sadness and frustration. Parents may be intimidated by the intensity of the suicidal behavior. They may adopt greater restrictiveness in their parenting style, or alternatively retreat to a position of minimal limit setting or try to transfer responsibility for their child to someone else (Hazell, 2000). How parents react to DSH may be influenced by factors such as the nature of the previous relationship with their son or daughter, the degree of suicidal intent involved in the act and whether the DSH act was a first episode or a repeat (Wagner, Aiken, Mullaley et al., 2000). The types of motives attributed to the act by parents, including whether the parents interpret the DSH as an act of manipulation, a sign of distress or a definite attempt to die, may also be important (James & Hawton, 1985). Outcome Following DSH Single Episode of DSH Compared With Those Who Repeat Some young people who harm themselves do so on only one occasion, whereas others repeat the behavior. Conceptually, the first act of self-harm is different from all those that follow it, and each act falls somewhere on the spectrum of suicidality in so far as many acts of self-harm have death as a possible outcome (either psychologically or medically). A history of previous suicidal behavior increases the risk of future attempts in both clinical and general populations (Evans, Hawton, & Rodham, 2004; Gould, Greenberg, Velting et al., 2003). The greatest risk of repetition is in the first year following DSH. The estimates of risk of repetition are 5–15% per year (Bridge, Goldstein, & Brent, 2006), although this may be much higher where repetition that does not come to clinical attention is considered (Hawton, Rodham, & Evans, 2006). The risk of repetition remains high for many years after an episode of DSH. For example, in a 10-year follow-up, Gibb, Beautrais, and Fergusson (2005) reported that 28% of those admitted for a suicide attempt had been readmitted, with the highest risk in the first 2 years. In a study of 450 adolescents who had taken overdoses, 12% re-presented to hospital with further overdoses within 5 years. Repetition is associated with substance abuse, psychotic illness and personality disorder (Reith, Whyte, & Carter, 2003). There are mixed findings on whether repetition rates are higher in one gender or the other (Gibb, Beautrais, & Fergusson, 2005; Goldacre & Hawton, 1985). Once an adolescent has actually engaged in DSH they cross a behavioral threshold. Repeat DSH may be more likely if the act resulted in the adolescent receiving relief from undesirable affect or if an earlier attempt prompted a desirable change in 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 657

times more frequent than expected. The main risk factors for suicide were male gender, previous DSH, prior psychiatric history and high suicide intent (Hawton & Harriss, 2007). Clinical Assessment Clinicians should conduct risk assessments when young people express suicidal thoughts or behaviors. Both the purpose and the process of such assessments need to be given careful consideration. A significant issue is establishing the purpose of the assessment, particularly suicide prediction compared with risk assessment (Bryan & Rudd, 2006). It is extremely difficult for clinicians to predict accurately the risk of their patient dying by suicide or of engaging in non-fatal suicidal behavior. An assessment should form the basis of future clinical management and establishing treatment goals. In adults, having a psychosocial assessment has been associated with reduced rates of repetition (Kapur, House, Dodgson et al., 2002). The fact that many adolescents spend very little, if any, time planning their deliberate self-harm (Rodham, Hawton, & Evans, 2004), and that being intoxicated is often associated with many such acts, compounds this issue (Esposito-Smythers & Spirito, 2004). A core task of a risk assessment is to establish an interactive and dynamic relationship; to be part of a response to the young person’s distress that offers some hope for a better future. Assessment following DSH Improved assessment and management of deliberate self-harm are highlighted in a number of published guidelines (American Academy of Child and Adolescent Psychiatry, 1999; National Institute for Clinical Excellence, 2004; Royal Australian and New Zealand College of Psychiatrists, 2004). The assessment of children and adolescents following DSH is influenced by a range of process and service issues. At a process level, the assessment of adolescents can present particular challenges, as young people are often ambivalent about their suicidality and fluctuating mood states can make it difficult to get clear information, particularly retrospectively. Current guidelines emphasize standards of care and note that several studies have suggested that some staff responsible for medical care have, or are perceived by DSH patients as having, negative attitudes towards those who deliberately harm themselves (Herron, Tichehurst, Appleby et al., 2001; Hopkins, 2002) and may not recognize the complex relationships between DSH and mental illness (Friedman, Newton, Coggan et al., 2006). Poor continuity of care requiring frequent repetition of their “story” (Dower, Donald, Kelly et al., 2000) and negative expectations about post-discharge therapy (Rotheram-Borus, Piacentini, Van Rossem et al., 1996) contribute to dissatisfaction among some adolescents who have self-harmed. In a study of adolescent DSH patients, those who were more satisfied with hospital management and subsequent therapy appeared to have better therapeutic outcomes (Burgess, Hawton, & Loveday, 1998). CHAPTER 40 658 their lives as a result of the responses of others. These factors plus further exposure to stressful life events and problems combine to place them at increased risk for engaging in DSH when facing similar situations; following the initial episode DSH becomes an additional tool in their behavioral repertoire where it did not exist previously (Goldston, Sergent Daniel, Reboussin et al., 1999). Depression is a key factor associated with repetition of DSH in adolescents (Hawton, Kingsbury, Steinhardt et al., 1999b). Similarly, self-reported DSH at age 12 years predicts suicidal ideation and DSH at 15 years (Sourander, Aromaa, Pihlakoski et al., 2006). A recent study by Harrington, Pickles, Aglan et al. (2006) showed that in most cases deliberate self-harm by adolescents ceased within 3 years. However, those who continued to self-harm into adulthood were characterized by higher rates of psychopathology and adversity in both childhood and adulthood; and, in another study, by anxiety, at least for females (Rudd, Joiner, & Rumzek, 2004). Emergence of Personality Disorders To date there has been little research on the prevalence and morbidity associated with personality disorders among adolescents. Borderline personality disorder (BPD) has long been associated with non-fatal DSH among adults, and some argue it takes a similar form in adolescents as seen with adults (Bradley, Conklin, & Westen, 2005). The use of this diagnosis in those under the age of 18 years is somewhat contentious (Vito, Ladame, & Orlandini, 1999). Worthlessness, guilt, hopelessness and anger are associated with both BPD and suicide (Apter & Freudenstein, 2000; Brodsky, Malone, Ellis et al., 1997) and may place young people at risk of poor psychosocial outcomes. In a communitybased longitudinal study, adolescents with personality disorders had significantly higher rates of major psychiatric disorder and suicidal ideation in early adulthood, after controlling for comorbid mental disorders and suicidality during adolescence (Johnson, Cohen, Skodol et al., 1999). Rudd, Joiner, & Rumzek (2004) suggested that the frequency and chronicity of suicide attempts in adulthood are related to childhood anxiety disorders through the emergence of personality psychopathology, with different patterns for males and females. The authors highlighted histrionic and paranoid traits in females and schizoid, avoidant, dependent, aggressive and borderline traits in males. Suicide Following DSH: Risk and Timing A history of past suicide attempts is one of the most powerful and clinically relevant predictors of eventual suicide. Most studies find elevated risk of overall mortality following DSH (Carter, Reith, Whyte et al., 2005; Gibb, Beautrais, & Fergusson, 2005; Goldacre & Hawton, 1985; Suominen, Isometsa, Suokas et al., 2004). In one follow-up study of 15- to 24-year-olds who had presented to hospital following an episode of DSH, the overall number of deaths from all causes was 3%, four times higher than expected. This was mainly because of an excess number of suicides (2%), which were 10 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 658

ments for DSH to offer a promising area for further investigation (Gaynes, West, Ford et al., 2004; Hawton, Townsend, Arensman et al., 2000; Townsend, Hawton, Altman et al., 2001). However, there have been no evaluations of problemsolving therapy with younger patients. Family Therapy Family therapy is a mechanism of intervening with suicide behavior among adolescents, given that family issues are implicated in the etiology of suicide behavior (Spirito & Boergers, 1997). Family therapy focuses on the relationships, roles and communication patterns between family members (see chapter 65). In a treatment study of depressed adolescents who were randomly allocated to CBT, systemic behavioral family therapy (SBFT) or non-directive supportive therapy (NST), those who were currently or previously suicidal were more depressed at the start of therapy and were significantly less likely to complete it. In addition, NST did not appear to ameliorate the MDD of these adolescents (Barbe, Bridge, Birmaher et al., 2004). Rotheram-Borus, Piacentini, Miller et al. (1994) developed brief CBT in a family context. Kerfoot, Harrington, and Dyer (1995) implemented a brief structured home-based intervention with suicidal adolescents and their families. Non-depressed adolescents in the home-based group had less suicidal ideation than controls, but the home-based intervention was no more effective for depressed adolescents (Harrington, Kerfoot, Dyer et al., 2000). Group Therapy Group therapy approaches are often used in child and adolescent mental health services, although there are few welldesigned studies of this approach with suicidal adolescents. Wood, Trainor, Rothwell et al. (2001) randomly assigned 63 adolescents with a history of repeated self-harm to group therapy plus treatment as usual (TAU) or TAU only. Although there was no apparent effect on depression, group attendees were less likely to repeat DSH, used fewer routine services and had better school attendance than those who received TAU. Dialectical Behavior Therapy Dialectical behavior therapy (DBT) is a therapeutic approach that focuses on the management of emotional states and interpersonal relationships. DBT has been researched as a psychotherapeutic intervention with suicidal adults (Linehan, Rizvi, Welch et al., 2000) and is being investigated with adolescents (Rathus & Miller, 2002). Multisystemic Therapy Multisystemic therapy (MST) was developed to treat delinquent youth, targeting the systems in which the young people live. MST includes parenting skills, family therapy and educational attainment. In a randomized controlled trial, young people aged 10–17 years were assigned to MST or hospitalization following a psychiatric emergency. MST was significantly more effective SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 659 Screening and Case Identification Procedures Some schools have tried to detect young people at high risk of suicide through screening programs. Case-finding strategies have been employed in schools in an effort to reduce suicide by early detection of young people at high risk. This approach has particularly been pursued in the USA (Gould, Greenberg, Velting et al., 2003). Although these methods are increasingly sensitive to detecting young people with problems, engagement in treatment following identification remains a significant issue (Shaffer & Craft, 1999; Shaffer & Pfeffer, 2001; Shaffer, Scott, Wilcox et al., 2004). Data from the Colombia Teen Screen program indicates that 19% of “at risk” young people refused a referral, 25% did not attend the first appointment and 17% attended one session only (Shaffer, 2003). There are also difficulties with some schools accepting this approach for various reasons, including lack of staff resources and concerns that asking students about suicide will give them ideas about harming themselves. However, in a recent randomized controlled trial, depressed adolescents and previous attempters reported lower levels of distress and suicidality following a screening questionnaire that included specific questions about suicidal behaviors compared with their counterparts who were not asked those questions. This study also demonstrated that asking about suicide does not “put the idea into a young person’s head” for those who would not ordinarily be thinking about this issue (Gould, Marrocco, Kleinman et al., 2005). Treatment Following DSH A range of treatment studies have been conducted with adults following DSH, but few interventions with children and adolescents who have harmed themselves have been evaluated. Cognitive–Behavior Therapy and Problem-Solving Cognitive–behavior therapy (CBT) is the principal treatment for adolescent depression and affective disorders (Harrington, Whittaker, & Shoebridge, 1998; Merry, McDowell, Hetrick et al., 2002) and targets depressive thoughts and behavior patterns (see chapter 63). In a large randomized controlled trial, 439 patients aged 12–17 years with major depressive disorder (MDD) were randomly allocated to one of four treatment conditions, each lasting 12 weeks: 1 Fluoxetine alone; 2 CBT alone; 3 CBT with fluoxetine; or 4 Placebo. The CBT treatment consisted of 15 1-hour sessions. Patients treated in all conditions showed a reduction in suicide ideation across the trial, those treated with CBT plus fluoxetine showing the greatest improvement (Treatment of Adolescent Depression Study Team, 2004). Problem-solving therapy, in which patients are assisted to identify problems and enhance their strategies for addressing them, has been noted in three recent systematic reviews of treat9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 659

in reducing youth-reported repetition of suicide attempts (Huey, Henggeler, Rowland et al., 2004). Medication There has been considerable recent debate about the use of antidepressant medications in the treatment of children and adolescents with depression, with a specific focus on whether selective serotonin reuptake inhibitors (SSRIs) increase the risk of suicidal behaviors in some young people (for summary see Ryan, 2005; see also chapters 37 and 67). A recent meta-analysis indicates a modest increased risk of suicidality among those prescribed antidepressant medication (Hammad, Laughren, & Racoosin, 2006). This may be related to the agitation that can occur shortly after starting the drug. In contrast, some researchers have suggested that increased prescribing of SSRIs has resulted in decreased suicide rates (Gibbons, Hur, Bhaumik et al., 2006; Olfson, Shaffer, Marcus et al., 2003). Conversely, based on data from both published and unpublished randomized controlled trials, the British Medicines and Healthcare Products Regulatory Agency has stated that sertraline, citalopram, paroxetine and venlafaxine are contraindicated in those under 18 years with MDD (Medicines and Healthcare Products Regulatory Agency, 2004). These medications are required to carry a “black box” warning label in the USA (US Food and Drug Administration, 2004). Also, fluoxetine for treating depression in adolescents is supported by the European Medicines Agency only where psychological interventions alone have failed (Eaton, 2006). The Society for Adolescent Medicine recommended the prudent use of antidepressant medication for adolescents, under close clinical supervision and as part of an overall therapeutic approach (Lock, Walker, Rickert et al., 2005; see also chapter 37). Hospitalization The decision to treat adolescents following DSH in an in-patient setting is usually based on risk of further self-harm and suicide, and severity of psychiatric disorder (Olfson, Gameroff, Marcus et al., 2005). It may also be influenced by other factors including concerns about litigation, characteristics of the individual and their family (Spooren, Jannes, & van Heeringen, 1997), the experience and training of the mental health clinician (Morrissey, Dicker, Abikoff et al., 1995) and the availability of in-patient beds. However, there is no evidence to suggest that hospitalization prevents young people, particularly those with prior attempts, mood disorder and substance abuse, from making another attempt or dying by suicide (Gould, Greenberg, Velting et al., 2003; Greenhill & Waslick, 1997). Furthermore, prior hospitalization for any injury, not just DSH, is associated with increased risk of suicidal behaviors (Agerbo, Nordentoft, & Mortensen, 2002; Bridge, Goldstein, & Brent, 2006), although this may be related to severity of psychopathology and other risk factors. Two recent studies have attempted to address these issues. In the first, conducted in the USA, 289 adolescents were randomly allocated to receive social network intervention plus TAU, or TAU alone, following psychiatric hospitalization. There was a reduction in suicidal ideation and parentreported functional impairment at 6 months follow-up in those assigned to social network intervention, but no effects on repetition of DSH or emotional symptoms (King, Kramer, Preuss et al., 2006). In the second study, 286 adolescents were assigned to rapid response out-patient follow-up or TAU following presentation to an emergency department in Canada. The results showed psychiatric hospitalizations can be prevented using the rapid response model of care (Greenfield, Larson, Hechtman et al., 2002). Issues of Access to Treatment and Engagement in Treatment Whereas many adolescents may be offered care following an episode of DSH, only a small proportion are successfully engaged in ongoing treatment. Treatment retention for nonhospitalized adolescents is generally below 50% (Brent, 1997; Swedo, 1989; van Heeringen, Jannes, Buylaert et al., 1995), and can be as low as 20%, with significant and rapid drop-out from treatment (King, Hovey, Brand et al., 1997). Several studies have investigated mechanisms to improve engagement with treatment, including green-card passes (Cotgrove, Zirinsky, Black et al., 1995), enhanced emergency department protocols (Rotheram-Borus, Piacentini, Cantwell et al., 2000; Spirito, Boergers, Donaldson et al., 2002), enhanced CBT interventions (Rotheram-Borus, Piacentini, Miller et al., 1994) and skills-based interventions (Donaldson, Spirito, & Esposito-Smythers, 2005). However, to date such efforts have largely been unsuccessful and new strategies must be developed to address this important issue (Burns, Dudley, Hazell et al., 2005). Many young people who engage in DSH do not seek help for their problems. If they do, it is most likely to be from friends and family rather than professionals (De Leo & Heller, 2004; Hawton, Rodham, & Evans, 2006). There are also gender differences, with distressed young men being less likely to seek help of any kind and those who seek help from their GP showing more severe symptoms than their female counterparts when they do (Biddle, Gunnell, Sharp et al., 2004). High school students at highest risk of suicide were found to be more likely to endorse isolative coping strategies such as believing you should be able to sort out your problems on your own and less likely to endorse strategies such as getting advice from friends (Gould, Velting, Kleinman et al., 2004). Prevention of DSH and Suicide by Children and Adolescents Suicide prevention strategies include both specific interventions for individuals at risk and population-level interventions aimed at reducing overall risk in the general population. Specific interventions include, for example, treatment and CHAPTER 40 660 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 660

prevention in North America because of the high number of deaths resulting from firearms (Brent, Perper, Goldstein et al., 1988; Brent, Baugher, Bridge et al., 1999; Gould, Greenberg, Velting et al., 2003). The number of firearms suicides in the UK is small so this does not form a major thrust of suicide prevention (Haw, Sutton, Simkin et al., 2004). Much suicidal behavior in young people involves intentional overdoses (Bennett, Coggan, Hooper et al., 2002; Hawton, Fagg, Simkin et al., 2000). Preventative approaches include safety packaging, limiting tablet quantity for high-risk drugs such as tricyclic antidepressants, education of practitioners regarding safer practices, disposal of out-of-date and unwanted drugs and limiting advertising (Cantor & Neulinger, 2000; Commonwealth Department of Health and Aged Care, 1999). Acetaminophen (paracetamol) is a drug widely used for selfpoisoning among young people in several western countries (Bennett, Coggan, Hooper et al., 2002; Hawton, Fagg, Simkin et al., 2000). Legislation was introduced in the UK in 1998 reducing pack sizes and the number of packs that can be purchased at one time. This was followed by a decrease in the rates of deaths, liver transplants and the average number of tablets ingested in overdose (Hawton, Simkin, Deeks et al., 2004). Hanging is an increasingly popular method of suicide and attempted suicide in several countries but it is difficult to reduce access to the means of hanging, except in institutional settings such as psychiatric in-patient units and prisons. Carbon monoxide poisoning from car exhaust gases was a common method of suicide. However, the introduction of catalytic converters in cars has had a significant impact in reducing deaths by this method (Amos, Appleby, & Kiernan, 2001). Crisis Centers and Hot Lines Crisis centers and hot lines offering direct counseling or links to mental health services are conceptually popular. Overall, research suggests that such services tend to be used by young White females, with less impact on young men (de Anda & Smith, 1993). Beautrais, Joyce, & Mulder, (1998) reported that 14% of serious suicide attempters had used a telephone crisis line in the year prior to their attempt. There is little evidence of beneficial effects on rates of suicide (Burns & Paton, 2000), although this would be difficult to demonstrate. Guidelines on Media Reporting of Suicides Media coverage of suicide has been shown to encourage imitative suicides (Gould, 2001; Hawton & Williams, 2005; Pirkis & Blood, 2001). It appears that in the short term, media reporting can lead to an increase in suicidal behavior and in the long term it may model suicide as common and acceptable. Many countries now have voluntary guidelines for media reporting (Pirkis, Blood, Beautrais et al., 2006a). Compliance with guidelines is variable although guidelines leading to reduced reporting of specific types of suicide have been associated with reduced rates of suicide by these methods in SUICIDAL BEHAVIOR AND DELIBERATE SELF-HARM 661 care of suicidal children or adolescents to help families and communities where a suicide death has occurred to cope with the aftermath (Leenaars & Wenckstern, 1999). Given the complicated nature of the lives of many people who engage in suicidal behavior, no single strategy is likely to provide all the answers (Centers for Disease Control and Prevention, 1992; Evans, 2000). School-based Interventions Prevention programs that are aimed at students as helpers, not as victims, are based on evidence that adolescents turn to their peers for support rather than discussing their problems with adults (Beautrais, Joyce, & Mulder, 1998; Hawton, Rodham, & Evans, 2006; Hazell & King, 1996). This approach often raises concerns that not all peer confidants communicate with adults about friends whose problems cause them particular concern (Bennett, Coggan, Lee et al., 2003) and that young men in particular do not respond to troubled peers in helping ways (Hazell & King, 1996; Kalafat, Elias, & Gara, 1993). Skills-based programs in schools, targeting the development of problem-solving, coping and cognitive skills appear to have a positive impact on suicide behavior and coping with distress (Gould, Greenberg, Velting et al., 2003). A schoolbased intervention in the USA called Signs of Suicide showed fewer suicide attempts in the intervention group compared with controls, and a modest improvement in knowledge and attitudes about depression and suicide. However, no improvement in help-seeking was observed (Aseltine & DeMartino, 2004). A randomized controlled trial of a school-based depression prevention program also showed positive results (Merry, McDowell, Wild et al., 2004). Reviews of older school-based programs (Garland, Shaffer, & Whittle, 1989) and their effect on suicidal adolescents (Shaffer, Vieland, Garland et al., 1990) raised serious concerns about these programs, in particular the message that suicide is a reaction to stressful life events that could happen to anyone and the minimization of the importance of mental illness, and gave rise to the establishment of the Columbia Teen Screen program. One obvious difficulty with any schoolbased program is the fact that high-risk individuals, particularly school drop-outs and those with high rates of absenteeism, will not be reached using this approach (Burns & Patton, 2000). Reducing Access to Methods of Suicide The strategy of restricting access by the general population to certain methods of suicide is a widely practized public health initiative and an effective method of preventing suicide. Research suggests that restricting access to particular methods reduces deaths by that method. Most studies show a reduction in overall suicide deaths, while others do not because of substitution of method (for a review see Mann, Apter, Bertolote et al., 2005). Methods of suicide used by young people vary significantly across different countries. Restricting access to firearms has been a significant focus of suicide 9781405145497_4_040.qxd 29/03/2008 02:52 PM Page 661

CHAPTER 40 662 Austria (Etzersdorfer, Sonneck, & Nagel-Kuess, 1992) and Canada (Littmann, 1983). Conclusions, Future Clinical and Research Directions Suicidal behavior exists on a continuum. Nearly 1 in 6 adolescents have considered self-harm or suicide in the previous year and 1 in 10 have harmed themselves in the previous year (Evans, Hawton, Rodham et al., 2005b). Death by suicide is relatively infrequent in adolescents. However, in most countries, more males than females die by suicide, although this may not be the case in India and China. In contrast, more females engage in non-fatal suicidal behavior. These differences are thought to reflect differences in the methods of deliberate self-harm utilized by males and females, although there is evidence that more violent methods, especially hanging, may be increasing in females. Acts of DSH are associated with a variety of motives or intentions. Wanting relief from unbearable feelings or situations, to die and to communicate distress are commonly endorsed motives in both hospital and community samples. Establishing the intent or motives associated with an episode of DSH by adolescents can be difficult. Using the method of DSH as a proxy for intent can be misleading; self-cutting and other methods of self-mutilation do not always involve suicidal intent, but some studies have found that young people who engage in cutting behaviors are at high risk of poor psychosocial outcomes and death by suicide. Community-based studies of adolescents indicate that cutting is the most frequently used method of DSH, whereas adolescents presenting to hospitals are most likely to have taken an overdose. Few differences exist, including in psychiatric symptomatology, between those who engage in self-harm by various methods. It is now clear that depression, sexual and physical abuse, substance abuse, hopelessness, family breakdown, poor coping, and suicidal behavior by family and friends and in the media increase the risk of suicidal phenomena among children and adolescents. Impulsivity and aggression are vulnerability factors that require further investigation. The role of emergent media forms such as cell phones and the Internet in suicide prevention and contagion is also an area in which one can expect research in the next few years. Relatively little research work has been conducted on factors that protect against the development of suicide behavior. Relevant factors appear to be social connectedness, problem-solving skills, an internal locus of control, involvement with school and recreational activities, life affirming beliefs and religious affiliation. Whereas many young people who harm themselves do so on only one occasion, others repeat the behavior. A history of previous suicidal behavior increases the risk of future attempts and suicide. The greatest risk of repetition is in the first year following DSH. The reasons why some young people, even those who experience multiple risk factors, stop self-harming require investigation. The core task of a risk assessment when young people express suicidal thoughts or behaviors is to establish an interactive and dynamic relationship and to be part of a response to the young person’s distress that offers some hope for a better future. Improved assessment and management of deliberate self-harm are highlighted in published guidelines. A number of key studies have evaluated treatment approaches, including CBT (with or without fluoxetine), MST and DBT. There has been considerable debate about the use of antidepressant medications in the treatment of children and adolescents with depression, with a specific focus on whether SSRIs increase the risk of suicidal behaviors in some young people. Antidepressants should only be used in adolescents when combined with psychological treatment. Further efforts are needed to improve engagement in treatment by children, adolescents and their families. Many young people who engage in DSH do not seek help for their problems. If they do it is most likely to be from friends and family in preference to formal helping agencies or professionals. There are also gender differences, with distressed young males being less likely to seek help of any kind. Suicide prevention strategies include specific interventions focused on high-risk groups, such as the management of suicide attempts, and population-level interventions such as restricting access to certain methods of suicide, school-based interventions targeted at the prevention of depression and equipping adolescents who are approached by a distressed peer to respond appropriately. 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670 The term “eating disorders” refers to anorexia nervosa and bulimia nervosa and their variants. These disorders typically develop in adolescence or early adulthood but in some cases they start earlier. They are not distinct conditions; they share much the same psychopathology and many patients migrate between them. The etiology of the eating disorders is complex and ill-understood and, with the exception of bulimia nervosa, there has been limited research on their treatment. Cases that present in childhood or adolescence have a fairly good prognosis, but those that persist into adulthood are generally selfperpetuating and difficult to treat. The prompt detection and treatment of childhood and adolescent cases are of paramount importance. Classification of Eating Disorders in Childhood and Adolescence The ICD and DSM schemes for classifying and diagnosing eating disorders are similar and recognize two main conditions: anorexia nervosa and bulimia nervosa. Where the schemes differ is in their classification of eating disorders other than anorexia nervosa and bulimia nervosa. In DSM-IV these states are placed in a single category termed “eating disorder not otherwise specified” (eating disorder NOS), whereas in ICD-10 a number of different eating disorder variants are recognized. In this chapter, the DSM-IV scheme is followed because it is more empirically based than ICD-10 and it is the one generally used in research. Eating disorders need to be distinguished from the DSM-IV diagnosis “feeding disorder of infancy or early childhood.” This refers to a persistent failure to eat adequately resulting in significant failure to gain weight or significant weight loss. The disturbance in eating should not be secondary to a general medical disorder or any other psychiatric condition, and its onset should be before the age of 6 years although typically it is much earlier (see chapter 53). More minor problems with feeding are common, especially in infancy, and faddy eating occurs in over 20% of preschool children. Some of the eating problems seen in late childhood or early adolescence are extensions of these earlier difficulties or variants on them. Various subtypes have been recognized including “food avoidance emotional disorder,” “selective eating,” “restrictive eating,” “food refusal” and “pervasive refusal” (Bryant-Waugh, 2000). In none of these states is there the overevaluation of shape and weight that characterizes anorexia nervosa and bulimia nervosa. Diagnostic Criteria In essence, three features need to be present to make a diagnosis of anorexia nervosa: 1 The overevaluation of shape and weight; that is, judging self-worth largely, or even exclusively, in terms of shape and weight. This is often expressed as an intense fear of becoming fat. 2 The active maintenance of an unduly low body weight (e.g., maintaining a body weight less than 85% of that expected, or a body mass index below the 2nd percentile for age). 3 Amenorrhea (in postpubertal females). The value of the amenorrhea criterion is questionable because the majority of female patients who meet the other two diagnostic criteria are amenorrheic, and those who do menstruate closely resemble those who do not. Three features also need to be present to make a diagnosis of bulimia nervosa: 1 The overevaluation of shape and weight, as in anorexia nervosa. 2 The presence of recurrent binge eating. A “binge” is an episode of eating during which there is a sense of loss of control and an objectively large amount of food is eaten. 3 The presence of extreme weight-control behavior, such as strict dietary restriction, recurrent self-induced vomiting or marked laxative misuse. It is also specified that the diagnostic criteria for anorexia nervosa should not be met because otherwise some patients would be eligible to receive both eating disorder diagnoses. There are no specific diagnostic criteria for eating disorder NOS. Instead, it is a residual category for eating disorders of clinical severity that do not meet the diagnostic criteria for anorexia nervosa or bulimia nervosa. Although neglected until recently, these states are common, both in adults and in children and adolescents. The relationship between the diagnoses anorexia nervosa, bulimia nervosa and eating disorder NOS is illustrated schematically in Fig. 41.1. Eating Disorders 41 Christopher G. Fairburn and Simon G. Gowers 9781405145497_4_041.qxd 1/04/2008 10:39 AM Page 670 Rutter’s Child and Adolescent Psychiatry, 5th Edition, Edited by M. Rutter, D. V. M. Bishop D. S. Pine, S. Scott, J. Stevenson, E. Taylor and A. Thapar © 2008 Blackwell Publishing Limited. ISBN: 978-1-405-14549-7

EATING DISORDERS 671 It has recently been proposed that an additional eating disorder be recognized, termed “binge eating disorder.” Because it is somewhat different in character to the other three eating disorders and mainly affects middle-aged adults, it will be discussed separately later in the chapter. Technically, binge eating disorder comes under the rubric of eating disorder NOS. Applying the diagnostic criteria for anorexia nervosa and bulimia nervosa to the clinical problems seen in children and adolescents poses certain problems. For example, some common clinical presentations do not fit the adult-oriented diagnostic criteria for eating disorders, this being particularly true of “anorexia nervosa” in children and younger adolescents. In this age group a significant number of those who are underweight because of purposeful undereating show no evidence of overconcern about shape or weight: rather, their dietary restriction appears to stem from an overevaluation of controlling eating per se. Strictly speaking, such patients should not be given the diagnosis of anorexia nervosa because a central diagnostic feature is not present. Instead, they should be given the diagnosis eating disorder NOS. Of course, it can be problematic identifying this psychopathology in younger patients because of the difficulty children have describing their thoughts, attitudes and behavior, combined sometimes with a reluctance to do so. Obtaining supplementary information from parents and other informants is essential and can be illuminating. The psychopathology of anorexia nervosa should never be inferred. Another problem centers on the weight criterion of anorexia nervosa because it is difficult to use with children and younger adolescents. This is for two main reasons: first, adult body mass index thresholds do not apply to younger age groups; and, second, growth may have been stunted. To address these problems it is advisable to compare the patient’s current centile for age, gender, weight and height with earlier ones if possible. The amenorrhea criterion also poses problems in premenarcheal cases who might be expected to have completed their puberty after the disturbance of eating began. In such cases it is best to ignore this feature. Clinical Features Anorexia nervosa and bulimia nervosa, and most cases of eating disorder NOS, share a distinctive “core psychopathology” which is essentially the same in females and males, adults and adolescents. This is the overevaluation of shape and weight. Whereas most people evaluate themselves on the basis of their perceived performance in a variety of domains of life (such as the quality of their relationships with their family and friends, their work, their sporting prowess), patients with anorexia nervosa or bulimia nervosa judge their self-worth largely, or even exclusively, in terms of their shape and weight and their ability to control them. This overevaluation of shape and weight results in a pursuit of weight loss – note it is weight loss that is sought, not a specific weight – and an intense fear of weight gain and fatness. Most of the other features of these disorders are secondary to this psychopathology and its consequences (e.g., undereating and being severely underweight). Thus, in anorexia nervosa there is a sustained and determined pursuit of weight loss and, to the extent that this pursuit is successful, this behavior is not seen as a problem. Indeed, it tends to be viewed as an accomplishment and, as a consequence, patients have a limited desire to change. In bulimia nervosa equivalent attempts to restrict food intake are punctuated by repeated episodes of binge eating with the result that patients may describe themselves as “failed anorexics.” The great majority of these patients are distressed by their loss of control over eating which makes them easier to engage in treatment, although because of the associated shame and secrecy there is typically a delay of many years before they seek help. This core psychopathology of anorexia nervosa and bulimia nervosa has other expressions too. Many patients mislabel adverse physical and emotional states as “feeling fat” and equate this with actually being fat. In addition, most repeatedly scrutinize aspects of their shape, focusing on parts that they dislike. This may contribute to them overestimating their size. Others actively avoid seeing their bodies, assuming that they look fat and disgusting. Equivalent behavior is seen with respect to weighing (weight checking) with most patients weighing themselves frequently and as a result becoming preoccupied with trivial day-to-day fluctuations, whereas others actively avoid knowing their weight while nevertheless being highly concerned about it. Anorexia Nervosa In anorexia nervosa the pursuit of weight loss is successful in that a very low weight is attained. This is primarily the result of a severe and selective restriction of food intake with foods viewed as fattening being excluded. Generally, there is no true “anorexia” as such. The undereating may also be an expression of other motives including asceticism and competitiveness with others. Some young people engage in a driven type of exercising which also contributes to their weight loss. Selfinduced vomiting and other forms of weight-control behavior (such as the misuse of laxatives or diuretics) are practiced by a subgroup, and an overlapping group have episodes of loss Fig. 41.1 A schematic representation of the relationship between the diagnoses anorexia nervosa, bulimia nervosa and eating disorder not otherwise specified (NOS). From Fairburn and Bohn (2005) with permission. Anorexia nervosa Bulimia nervosa Eating disorder NOS Not a “case” Eating disorder “case” Not a “case” 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 671

of control over eating although the amount eaten is often not objectively large (subjective binge eating). Depressive and anxiety features, irritability, lability of mood, impaired concentration, loss of sexual appetite and obsessional symptoms are frequently present. Typically, these features get worse as weight is lost and improve with weight regain. Interest in the outside world also declines as patients become underweight with the result that most become socially withdrawn and isolated. This too tends to reverse with weight regain. Bulimia Nervosa The eating habits of young people with bulimia nervosa resemble those seen in anorexia nervosa. The main distinguishing feature is that the attempts to restrict food intake are punctuated by repeated episodes of binge eating. The amount consumed in these binges varies but is typically 1000–2000 kcal per episode, and their frequency ranges from once or twice a week (the diagnostic threshold) to many times a day. In most cases, each binge is followed by compensatory self-induced vomiting or laxative misuse but there is a subgroup who do not “purge.” The weight of most of these patients is in the healthy range (equivalent to a body mass index of 20–25 in an adult) because the effects of the undereating and overeating cancel each other out. As a result, patients with bulimia nervosa do not experience the secondary psychosocial and physical effects of maintaining a very low weight. Depressive and anxiety symptoms are prominent in bulimia nervosa – indeed, more so than in anorexia nervosa – and there is a subgroup who engage in substance misuse or self-injury or both. This subgroup, which is also present among those anorexia nervosa patients who binge eat, is probably overrepresented in specialist treatment centers. Eating Disorder NOS The psychopathology of eating disorder NOS closely resembles that seen in anorexia nervosa and bulimia nervosa, albeit the various clinical features are present at somewhat different levels or in different combinations (Fairburn & Bohn, 2005). Many adult cases of eating disorder NOS have had frank anorexia nervosa or bulimia nervosa in the past, their present state being simply the latest expression of an evolving eating disorder. Equivalent information on course has yet to be reported in adolescents. It is helpful to distinguish two subgroups within eating disorder NOS, although there is no sharp boundary between them. The first comprises cases that closely resemble anorexia nervosa or bulimia nervosa but just fail to meet their diagnostic thresholds (e.g., body weight may be marginally above the limit for anorexia nervosa or the frequency of binge eating may be just too low for a diagnosis of bulimia nervosa). These cases may be classed as “subthreshold” forms of anorexia nervosa or bulimia nervosa, respectively, and should generally be managed as such. In the second group are cases in which the clinical features of anorexia nervosa and bulimia nervosa are combined in a different way to that seen in these two disorders. Such states may be described as “mixed” in character. Other terms have been used to describe the clinical presentations seen in eating disorder NOS including “subclinical” for the former subgroup, a term that is inappropriate given that these states are of clinical severity; and “atypical” or “partial” for the second subgroup. Both the latter terms are problematic; the first because these states are common and the second because of the implication that they are less severe than the full syndromes. Distribution There is limited reliable information on the distribution of eating disorders and the data that do exist come from studies of western samples. Virtually nothing is known about the distribution of eating disorders in non-western countries. Within western samples, most is known about the distribution of eating disorders among young adults. There have been few studies of children and adolescents, and the findings to date must therefore be regarded as tentative and imprecise (Commission on Adolescent Eating Disorders, 2005). What is clear is that anorexia nervosa is rare. Most estimates of the point prevalence of anorexia nervosa come from studies of adolescent girls or young adult women, the group thought to be at greatest risk. Even within this group, the prevalence figures obtained are low at 0–0.9% (Hoek, 2006). Outside this age group, and in boys and men, anorexia nervosa is likely to be even less common. Figures for the incidence of anorexia nervosa are particularly suspect as most are based on cases detected medically. They suggest that anorexia nervosa has become more common over recent decades, and especially so in adolescent females, but the apparent increase could well be because of greater help-seeking, better detection and changes in diagnostic practice rather than any true increase in the incidence of the disorder (van Son, van Hoeken, Bartelds,van Furth, & Hoek, 2006). In clinical samples, anorexia nervosa is the least common of the three eating disorder diagnoses, comprising 10–15% of adult cases. In adolescent samples the proportion is higher (Nicholls, Chater, & Lask, 2000). The ratio of females : males is about 10:1 in adults but it appears to be somewhat lower in adolescents (Doyle & Bryant-Waugh, 2000). Unlike anorexia nervosa, epidemiological data indicate that bulimia nervosa is more a disorder of early adulthood than adolescence, with most patients being in their twenties (Fairburn, Welch, Doll, Davies, & O’Connor, 1997; Hoek & van Hoeken, 2006). It is more common than anorexia nervosa, in part because the age group at risk is broader (18- to 40-year-old women) and in part because the point prevalence rate is higher (1.0–2.0%). There are no reliable data on the prevalence of bulimia nervosa in boys or men. Clinical experience suggests that bulimia nervosa became considerably more common in the 1970s and 1980s, and limited epidemiological data support this, although there is evidence that the rise has now ceased (van Son, van Hoeken, Bartelds et al., 2006). The explanation for these changes is not clear. What CHAPTER 41 672 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 672

is known is that most cases of bulimia nervosa are not in treatment and the subgroup that is receiving help is atypical in that the eating disorder is more severe and there is greater psychiatric comorbidity (Fairburn, Welch, Norman et al., 1996). Within clinical samples male cases are unusual. Bulimia nervosa comprises about 30–40% of adult eating disorder cases. The most glaring gap in knowledge about the epidemiology of eating disorders is the total absence of reliable data on the prevalence and incidence of eating disorder NOS in community samples (Hoek, 2006). Studies of adolescents and young adults often report detecting large numbers of people with “partial” or “atypical” syndromes but the status of these cases is unclear in the absence of an agreed definition of eating disorder NOS. What is now well-established is that eating disorder NOS is the most common eating disorder diagnosis among adults, comprising 50–60% of cases (Fairburn & Bohn, 2005) and the same is true of adolescents (Nicholls, Chater, & Lask, 2000). As with anorexia nervosa and bulimia nervosa, it is females who are primarily affected. Development and Subsequent Course Eating disorders typically develop in adolescence and therefore in the context of “normative” concerns about shape, weight and eating. Physical self-consciousness is common as adolescents come to terms with the changes in their shape that occur at puberty; early pubertal development in girls being associated with especially high rates of body dissatisfaction. Many children, particularly girls, believe that thinness is important to attractiveness, and academic and social success. Even small children believe that fat is undesirable, and girls have been found to prefer thin rather than fat girls as friends. It is therefore not surprising that dieting is common among adolescent girls. This said, there are distinct differences between the behavior and concerns of teenage girls and the psychopathology of people with eating disorders. For example, teenage dieting tends to be intermittent, flexible and not particularly strict, whereas the dietary restraint and restriction of people with eating disorders are persistent, rigid and extreme. While many teenage girls are dissatisfied with their appearance, few show the core psychopathology of eating disorders (i.e., the judging of their selfworth largely, or even exclusively, in terms of their shape and weight). Also, behaviors such as binge eating (as technically defined), self-induced vomiting, laxative misuse and driven exercising are unusual outside those with a frank eating disorder. The relationship between normative dieting and the development of an eating disorder is ill-understood (for further consideration of this topic see chapter 13). Whereas many adolescent girls diet, few develop an eating disorder of clinical severity. Controlled community-based risk-factor studies have shown that those who develop anorexia nervosa or bulimia nervosa have not only been exposed to circumstances that are likely to increase their risk of dieting (e.g., presence of dieting and weight concern in the family, and a history of childhood obesity in the case of bulimia nervosa), but they have also raised rates of exposure to risk factors for other psychiatric disorders (e.g., family history of depression, adverse childhood experiences including sexual abuse). In addition, premorbid negative self-evaluation and perfectionism are common (Fairburn, Welch, Dou et al., 1997; Fairburn, Cooper, Doll et al., 1999; Fairburn, Cowen, & Harrison, 1999). Thus, it is thought that dieting and shape concern, together with other general psychiatric vulnerability factors, put people at risk of developing an eating disorder. As yet, there have been no satisfactory prospective studies of the development of eating disorders so the findings of the risk-factor research have not been corroborated (Jacobi, 2005). Longitudinal studies such as the Dunedin multidisciplinary health and development study (Arsenault, Moffitt, Caspi et al., 2000; Silva & Stanton, 1997) have the potential to do this and indeed 1.4% of the females in this large cohort had developed an eating disorder by the age of 21 years. However, such studies have been unable to differentiate between risk factors for dieting (e.g., body dissatisfaction), which is an extremely common behavior of no psychopathological significance, and those for clinical eating disorders, which are uncommon. Fairburn, Cooper, Doll et al. (2005) followed almost 3000 16- to 23-year-old dieters over 2 years to determine the characteristics of those who would go on to develop an eating disorder. As expected, only a small proportion of the dieters developed an eating disorder. Not surprisingly, the dieters who developed an eating disorder had more disturbed eating habits and attitudes at baseline than those who did not. Also unsurprising was the fact that several of the features that best identified future cases were features seen in people with eating disorders albeit to a much greater extent (e.g., binge eating, purging and being underweight). Other ominous features were less predictable: eating in secret; preoccupation with food, eating, shape, or weight; fear of losing control over eating; and wanting to have a completely empty stomach. There are data that suggest that eating disorders are more common than would be expected among models and ballet dancers. It is debatable whether this is as a result of the occupational pressure to be thin, because clinical experience suggests that people who are already concerned about their appearance may be particularly attracted to such careers. Anorexia Nervosa Anorexia nervosa generally starts as teenage dieting which becomes progressively more extreme and out of control. Often the disorder is short-lived and self-limiting, or it only requires a brief intervention. This is most typical of young cases with a short history. In other cases, it becomes entrenched and may require intensive treatment. Recent outcome studies in which adolescents have been followed-up after 10 years or more report a good outcome in 49–76% of cases, an intermediate outcome in 11–41%, and a poor outcome in 8–14% (Råstam, Gillberg, & Wentz, 2003; Strober, Freeman, & Morrell, 1997). In adults, less than half of cases have a good outcome (Steinhausen, 2002). This heterogeneity in outcome is often neglected in accounts of the disorder. Even after successful treatment, some residual features are common, particularly a degree of over concern about shape, EATING DISORDERS 673 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 673

weight and eating. In cases that persist a frequent occurrence is the development of binge eating and frank bulimia nervosa. Most prominent among the favorable prognostic factors are an early age of onset and a short history, whereas unfavorable factors include a long history, severe weight loss and vomiting. This said, the prognostic significance of age of onset is inconsistent (Steinhausen, 2002), possibly because the earlyonset cases comprise two groups with different outcomes; the prepubertal cases having a poor prognosis whereas the others have a relatively good outcome (Russell, 1992). Anorexia nervosa is the one eating disorder to be associated with a raised mortality rate, anorexia nervosa patients being 12 times more likely to die than women of a similar age in the general population (Keel, Dorer, Eddy et al., 2003). The mortality rate among adolescents is low. Most deaths are either a direct result of medical complications or from suicide. The outcome in terms of the presence of other psychiatric disorders generally fails to distinguish between those present at the time of diagnosis, which may influence outcome, from those that develop later on. A systematic review of 119 outcome studies found high rates of anxiety disorders and affective disorders at follow-up (Steinhausen, 2002). Difficulties with social and personality functioning are often reported, as are negative physical outcomes such as failure to reach expected height, stunted breast development and reduced bone density. Whereas a range of Axis 1 psychiatric disorders and personality disorders have been reported at long-term follow-up, these appear to be largely absent in those whose eating disorder has fully remitted. In the longer term, eating disorders may have an impact on pregnancy and motherhood. In those recovering from anorexia nervosa, fertility problems, spontaneous abortion, prematurity and small-for-dates babies are regularly reported, as are elevated rates of infant mortality (Key, Mason, & Bolton, 2000; Zipfel, Lowe, & Herzog, 2003). In bulimia nervosa, symptoms often improve during pregnancy and in the period after birth, because of the mother’s attempts to exert behavioral control over her eating for the good of the child. Nevertheless, women with bulimia nervosa are at risk of having small babies and higher rates of Cesarean section. Concerns have been expressed about the parenting abilities of mothers with eating disorders, particularly with respect to difficulties managing infants’ meal times and play. A number have been shown to be intrusive and controlling, and they may have difficulty tolerating messy foods and activities resulting in a strained emotional atmosphere around meal times (Stein, Woolley, & Murray, 2001). Bulimia Nervosa Both community and clinic-based studies indicate that bulimia nervosa has a somewhat later age of onset than anorexia nervosa although it usually starts in much the same way: indeed, in about one-quarter of cases the diagnostic criteria for anorexia nervosa are met for a time. Eventually, however, episodes of binge eating begin to interrupt the dietary restriction and as a result body weight rises to normal or near normal levels. The disorder is remarkably self-perpetuating once established. Adult patients generally present with a 5–10-year history of unremitting symptoms, and even 5–10 years after presentation between one-third and half still have an eating disorder of clinical severity although in many cases it has evolved into a form of eating disorder NOS (Keel, Mitchell, Miller, Davis, & Crow, 1999). A large-scale prospective study of cases in the community indicated that they have a similarly poor prognosis (Fairburn, Cooper, Doll, Norman, & O’Connor, 2000). Mortality rate does not appear to be raised in bulimia nervosa (Keel Dorer, Eddy et al., 2003). No consistent predictors of outcome have been identified, although childhood obesity, low self-esteem and personality disturbance are often associated with a worse prognosis. The course of bulimia nervosa in adolescence has not been studied. Eating Disorder NOS The course of eating disorder NOS has barely been studied. As with bulimia nervosa, a 5–10-year history of unremitting symptoms is the norm among adult cases with many patients having a history of anorexia nervosa or bulimia nervosa. When a longitudinal perspective is taken, the distinctiveness of the three eating disorder diagnoses begins to break down. Most patients with an eating disorder migrate between these diagnoses, and from their perspective they have had one evolving eating problem. This temporal movement, together with the fact that anorexia nervosa, bulimia nervosa and eating disorder NOS share much the same distinctive psychopathology, suggests that common mechanisms are involved in the persistence of these disorders (Fairburn, Cooper, & Shafran, 2003). However, the fact that eating disorders do not evolve into other conditions supports the distinctiveness of the diagnostic category as a whole. Etiology Research on the etiology of the eating disorders has focused almost exclusively on anorexia nervosa and bulimia nervosa. It is clear that there is a genetic predisposition and a range of environmental risk factors, and there is some information regarding the identity and relative importance of these contributions. However, virtually nothing is known about the individual causal processes involved or how they interact and vary across the development and maintenance of these disorders. Genetic Factors Eating disorders and certain associated traits run in families with there being cross-transmission between anorexia nervosa, bulimia nervosa and eating disorder NOS (Strober, Freeman, Lampert, Diamond, & Kaye, 2000). This suggests that there is a shared familial liability. There is a raised prevalence of depression in these families, the pattern of familial transmission being unclear (Lilenfeld, Kaye, Greeno et al., 1998). The prevalence of substance abuse is also increased, especially among the relatives of bulimic probands, but in this case there seems CHAPTER 41 674 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 674

to be no cross-transmission (Lilenfeld, Kaye, Greeno et al., 1998). In addition, there is evidence of familial coaggregation of anorexia nervosa and obsessional and perfectionist traits (Lilenfeld, Kaye, Greeno et al., 1998). In the absence of adoption studies, twin designs have been used to establish the extent of the genetic contribution to the familiality of eating disorders (Slof-Op ’t Landt, van Furth, Meulenbelt et al., 2005). Clinic samples show concordance for anorexia nervosa of around 55% in monozygotic twins and 5% in dizygotic twins, with the corresponding figures for bulimia nervosa being 35% and 30%, respectively (Bulik, Sullivan, Wade, & Kendler, 2000; Fairburn, Cowen, & Harrison, 1999). These findings suggest a significant heritability of anorexia nervosa but not bulimia nervosa. Because clinic-based samples are potentially biased, population-based studies have also been conducted. These have used broader phenotypes because of the relative rarity of these disorders, and varied findings have emerged. As a result there is still uncertainty as to the extent of the genetic contribution to anorexia nervosa and bulimia nervosa, with there being differing point estimates and wide confidence intervals. The same applies to the contributions of individual-specific and shared (common) environmental factors. There is some evidence that the magnitude of the genetic contribution may increase during adolescence (Klump, McGue, & Iacono, 2003). Given the clear and possibly substantial genetic contribution to both anorexia nervosa and bulimia nervosa, molecular genetic studies have been conducted to identify the underlying loci and genes. Genetic association studies have focused in particular on polymorphisms in 5-HT (serotonin) related genes because this neurotransmitter system is important in the regulation of eating and mood, but a range of other polymorphisms have also been investigated. Despite this, no associations with eating disorders have been clearly replicated or confirmed in a family study or by meta-analysis. There has been one multicenter genome-wide linkage study. It found linkage peaks for anorexia nervosa and bulimia nervosa on chromosomes 1, 4, 10 and 14. A further analysis, which covaried for related behavioral traits, identified a different locus on chromosome 1, as well as loci on chromosomes 2 and 13. All these findings await replication. Other Risk Factors Many other risk factors have been implicated in clinic and community-based case–control studies (Commission on Adolescent Eating Disorders, 2005; Jacobi, Hayward, de Zwaan, Kraemer, & Agras, 2004). Satisfactory prospective studies are lacking, in part because of the rarity of these disorders. The main putative risk factors are listed in Table 41.1. These differ in the nature, strength and specificity of their association with individual eating disorders. Some are adverse premorbid experiences of the type associated with many psychiatric disorders (e.g., childhood sexual abuse), there being no specific association with eating disorders. Others are common to anorexia nervosa and bulimia nervosa (e.g., parental concerns about shape and weight; a family history of a frank eating disorder; EATING DISORDERS 675 see chapter 27), whereas others appear to predispose especially to bulimia nervosa (e.g., childhood and parental obesity, early menarche, parental alcoholism). Certain of these factors are likely to operate by sensitizing the person to her or his shape thereby encouraging dieting, an effect that is most likely to be seen in women in western societies in view of the social pressure on them to be slim. Yet other risk factors are character traits, the two most prominent being low self-esteem and perfectionism, the latter being a particularly common antecedent of anorexia nervosa. There have been no studies of protective factors. There is limited information on the distribution and form of eating disorders in non-western societies (Becker & Fay, 2006). There is no doubt that eating disorders occur in most societies, but their relative prevalence is not known. Within western societies there is evidence that some ethnic minority groups may be equally at risk of developing an eating disorder as their White peers. Aspects of the psychopathology of eating disorders may differ in non-western cases. For example, it has been noted that Chinese patients with “anorexia nervosa” often do not show the pathognomonic overevaluation of shape and weight; rather, their purposeful weight loss appears to result from other motives. Similarly, there is evidence that British Asian patients have less marked shape concerns than their Table 41.1 Main putative risk factors for anorexia nervosa and bulimia nervosa. After Fairburn and Harrison (2003). General factors Female Adolescence and early adulthood Living in a western society Individual-specific factors Family history • Eating disorder of any type • Depression • Substance abuse, especially alcoholism (bulimia nervosa) • Obesity (bulimia nervosa) Premorbid experiences • Adverse parenting (especially low contact, high expectations, parental discord) • Sexual and physical abuse • Family dieting • Critical comments about eating, shape or weight from family and others • Occupational and recreational pressure to be slim (e.g., ballet dancing) Premorbid characteristics • Low self-esteem • Perfectionism (anorexia nervosa and to a lesser extent bulimia nervosa) • Anxiety disorders (especially social phobia and obsessivecompulsive disorder) • Obesity (bulimia nervosa) • Early menarche (bulimia nervosa) 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 675

British White counterparts. It has been proposed that bulimia nervosa may be more culturally determined than anorexia nervosa and that heritability estimates for bulimia nervosa may therefore show greater cross-cultural variability than those for anorexia nervosa (Keel & Klump, 2003). Neurobiological Findings There has been extensive research on the neurobiology of eating disorders. This has mainly focused on the neuropeptide and monoamine (especially 5-HT) systems thought to be central to the physiology of eating and weight regulation (Kaye, Frank, Bailer et al., 2005). Of the various central and peripheral abnormalities reported, many are likely to be secondary to the disturbance of eating and associated weight loss. However, some aspects of 5-HT function remain abnormal after recovery, leading to speculation that there is a trait monoamine abnormality that may predispose to the development of eating disorders or to associated characteristics such as perfectionism. Furthermore, normal dieting in healthy women alters central 5-HT function, providing a potential mechanism by which eating disorders might be precipitated in women vulnerable for other reasons. Brain imaging studies have identified altered activity in the frontal, cingulate, temporal and parietal cortical regions in both anorexia nervosa and bulimia nervosa, and there is some evidence that these alterations persist after recovery (Kaye, Wagner, Frank, & Bailer, 2006). Whether they are a consequence of the eating disorder (i.e., a “scar”) or have somehow contributed to it is not known. It is important to stress that the findings to date have not been consistent. The eating disorder field has somewhat lagged behind others in terms of brain imaging research. Postulated Psychological Processes Specific psychological theories have been proposed to account for the development and maintenance of eating disorders. Most influential in terms of treatment have been cognitive– behavioral theories. In brief, these propose that the restriction of food intake that characterizes the onset of many eating disorders has two main origins, both of which may operate in an individual case. The first is a need to feel “in control” of life which gets displaced on to controlling eating. This need for control may be greatest in those who are constitutionally anxious, perfectionist or lacking in self-esteem. The second is an overevaluation of shape and weight in those who have been sensitized to their appearance, either by prior experiences (e.g., childhood obesity, parental concerns about eating) or by the changes in shape that occur during puberty. In both instances, the resulting dietary restriction and weight loss are highly reinforcing. Subsequently, other processes begin to operate and serve to maintain the eating disorder. These differ according to the form of the eating disorder. In patients who are severely underweight certain of the so-called “starvation symptoms” have this effect, particularly the preoccupation with food and eating, heightened fullness because of delayed gastric emptying, and social withdrawal. In patients who are binge eating and vomiting, other maintaining mechanisms operate. For example, rigid dietary restraint increases the likelihood of binge eating which in turn encourages further dietary restraint. Self-induced vomiting, while used to compensate for binge eating, results in the binges becoming larger and more frequent. External processes are important too. In those who are primarily restricting their eating, interpersonal conflict (e.g., family arguments) and other forms of stress (e.g., school examinations) tend to lead to an intensification of the dietary restriction thereby bolstering the person’s sense of self-control. In those prone to binge eat, adverse events and negative moods may trigger episodes of binge eating, the binges tending to modulate the negative mood and distract the person from the problem at hand. These processes are described in more detail in cognitive–behavioral accounts of eating disorders (Fairburn, 2006). Binge Eating Disorder In comparison to anorexia nervosa and bulimia nervosa, little is known about binge eating disorder. Although it shares with bulimia nervosa the phenomenon of binge eating, its overlap with the other eating disorders is limited: most patients are middle-aged, the gender ratio is less uneven, and the binge eating occurs against the background of a general tendency to overeat rather than dietary restraint (which probably accounts for its strong association with obesity). Furthermore, findings from natural history studies and drug trials suggest that there is a high spontaneous remission rate, unlike the other eating disorders seen in adults. Binge eating disorder does occur in adolescence, generally in combination with obesity, and it is likely to be a risk factor for weight gain. Table 41.2 summarizes current knowledge about the disorder. Medical Complications and their Management Most of the physical abnormalities seen in anorexia nervosa are thought to be caused by these patients’ disturbed eating habits and the resulting low weight. Hence, the great majority are reversed by treatment focused on establishing healthy eating habits and a normal weight. The principal physical features are listed in Table 41.3. The physical abnormalities found in bulimia nervosa are usually minor unless purging (vomiting or laxative or diuretic misuse) is frequent, in which case there is risk of fluid and electrolyte disturbance. Those patients who vomit frequently are also at risk of dental damage. The physical abnormalities found in eating disorder NOS depend on the nature of the eating disturbance and the patient’s weight. There are no established medical complications of binge eating disorder per se (other than those secondary to comorbid obesity). Most of the medical complications occur with equal frequency in adults and adolescents. Some points need to be stressed, CHAPTER 41 676 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 676

EATING DISORDERS 677 however, when considering adolescents (Commission on Adolescent Eating Disorders, 2005). First, young adolescents have incomplete stores of body fat and other substrates and as a result experience major medical complications after relatively small amounts of weight loss. Second, when anorexia nervosa develops prior to the completion of growth it can result in growth retardation and short stature. This is especially likely in boys because boys grow, on average, for 2 years longer than girls. Catch-up growth can occur with nutritional rehabilitation but nevertheless these adolescents may never reach their height potential. Third, pubertal delay frequently occurs among those who develop the disorder prior to the completion of puberty. Weight gain and the establishment of healthy eating habits usually result in the resumption of spontaneous menstruation but in some cases the amenorrhea may be prolonged. Fourth, the osteopenia and osteoporosis of anorexia nervosa are especially relevant to this age group because adolescence is a critical time for bone mass acquisition. Those who develop anorexia nervosa during adolescence are unlikely to reach their optimal peak bone mass with the consequence that they may be at heightened fracture risk for many years even if they recover from the eating disorder. The underlying pathophysiology is ill-understood and there is uncertainty over the best form of treatment. Restoration of healthy eating habits and weight, and an adequate diet, and with them the resumption of spontaneous menstruation, are of central importance. It is also usual to prescribe calcium supplements, generally given as a multimineral preparation. Hormone replacement therapy is not recommended because there is no evidence that it is effective and there is a risk that it might cause premature closure of the epiphyses. The panoply of physical abnormalities seen in the eating disorders can cloud thinking about diagnosis and management. The diagnosis of an eating disorder is made on positive grounds by using the history and mental state examination to detect the characteristic behavioral and attitudinal features, not by simply ruling out possible physical causes. No laboratory tests are required to make the diagnosis and, unless there are positive reasons to suspect the presence of physical disease, no tests are required to exclude other medical disorders. In general, the management of any physical abnormalities should focus on the correction of the eating disorder. However, lifethreatening complications must be addressed and the patient’s nutritional state needs to be optimized. Definition Recurrent episodes of binge eating in the absence of extreme weight-control behavior. Binge eating disorder is subsumed under the diagnosis eating disorder NOS Clinical features Frequent binge eating, much as in bulimia nervosa, but against the background of a general tendency to overeat. Strong association with obesity. By definition, self-induced vomiting and laxative misuse are not present or only occasional. Depressive features and dissatisfaction with shape are present, although they tend to be less severe than in bulimia nervosa Distribution Patients typically present in their forties and as many as one-third are male. Prevalence in the community has not been satisfactorily established. Present in 5–10% of adults seeking treatment for obesity Pathogenesis Barely studied. Lower exposure to “eating disorder risk factors” than in anorexia nervosa and bulimia nervosa. Nature of relationship with obesity unclear Course Little known. Patients typically give long histories of being prone to binge eat, particularly at times of stress, but many also report extended periods free from binge eating. Spontaneous remission rate appears high Medical complications None established other than those secondary to comorbid obesity Response to treatment In the short term, binge eating disorder appears more treatment-responsive than anorexia nervosa and bulimia nervosa. Notable placebo response rate. Frequency of binge eating declines in response to a variety of pharmacological and psychological treatments, including cognitive–behavior therapy, interpersonal psychotherapy, behavioral weight loss programs and self-help but with little accompanying weight change. No studies of long-term course or outcome Table 41.2 Current knowledge about binge eating disorder. After Fairburn and Harrison (2003). 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 677

CHAPTER 41 678 Management of Eating Disorders Research Evidence There has been very little research on the treatment of anorexia nervosa but most of the work that has been carried out has concerned adolescents. There has been much more research on the treatment of bulimia nervosa but so far it has focused exclusively on adults (Commission on Adolescent Eating Disorders, 2005; National Institute for Clinical Excellence, 2004). Physical symptoms Heightened sensitivity to cold Gastrointestinal symptoms (e.g., constipation, fullness after eating, bloatedness) Dizziness and syncope Amenorrhea (in females not taking an oral contraceptive); low sexual appetite; infertility Poor sleep with early morning wakening Physical signs Emaciation; stunted growth and failure of breast development (if prepubertal onset) Dry skin; fine downy hair (lanugo) on the back, forearms and side of the face; in patients with hypercarotenemia, orange discoloration of the skin of the palms and soles Swelling of parotid and submandibular glands (especially in bulimic patients) Erosion of inner surface of front teeth (perimylolysis) in those who vomit frequently Cold hands and feet; hypothermia Bradycardia; orthostatic hypotension; cardiac arrhythmias (especially in underweight patients and those with electrolyte abnormalities) Dependent edema (complicating the evaluation of body weight) Weak proximal muscles (elicited as difficulty rising from a squatting position) Abnormalities on physical investigation Endocrine Low LH, FSH and estradiol Low T3, T4 in low normal range, normal TSH (“low T3 syndrome”) Mild elevation of plasma cortisol Elevated growth hormone Severe hypoglycemia (rare) Low leptin (but possibly higher than would be expected for body weight) Cardiovascular ECG abnormalities (especially in those with electrolyte disturbance): conduction defects, especially prolongation of the Q-T interval, of major concern Gastrointestinal Delayed gastric emptying Decreased colonic motility (secondary to chronic laxative misuse) Acute gastric dilatation (rare, secondary to binge eating or excessive refeeding) Hematological Moderate normocytic normochromic anemia Mild leucopenia with relative lymphocytosis Thrombocytopenia Other metabolic abnormalities Hypercholesterolemia Increased serum carotene Hypophosphatemia (exaggerated during refeeding) Dehydration Electrolyte disturbance (varied in form; present in those who vomit frequently or misuse large quantities of laxatives or diuretics): vomiting – metabolic alkalosis and hypokalemia; laxative misuse – metabolic acidosis, hyponatremia, hypokalemia Other abnormalities Osteopenia and osteoporosis (with heightened fracture risk) Enlarged cerebral ventricles and external cerebrospinal fluid spaces (pseudoatrophy) ECG, electrocardiogram; FSH, follicle-stimulating hormone; LH, luteinizing hormone; TSH, thyroid-stimulating hormone. Table 41.3 Principal physical features of anorexia nervosa. After Fairburn and Harrison (2003). 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 678

One general point is worth stressing at the outset. Treatment outcome among adolescents with anorexia nervosa is generally good, in marked contrast with that amongst adults (Deter, Schellberg, Köpp, Friederich, & Herzog, 2005). This is probably an inherent property of the disorder in these two age groups rather than a reflection of the potency of the treatments used. Adolescents with anorexia nervosa tend to have had the disorder for a very short time – often little more than a year – whereas adults generally have a history of 5 or more years of unremitting symptoms. Thus, many of the maintaining mechanisms that obstruct change in the more enduring cases may not yet be operating in younger patients with the result that they are more responsive to treatment. The same is likely to be true of adolescent cases of bulimia nervosa and eating disorder NOS. Accordingly, priority should be given to the detection and treatment of eating disorders in adolescence in order to prevent them becoming established and progressively more treatment-resistant. Anorexia Nervosa There is a range of treatment options for anorexia nervosa. There are various treatment settings, the main ones being outpatient, day patient (partial hospitalization) and in-patient treatment; and within these settings a variety of interventions may be provided, pharmacological or psychological or both. To complicate matters, patients may move from one setting to another, and within any one setting often more than one treatment is employed. There is no empirical evidence to support the use of any one treatment setting over any other in terms of treatment outcome. There has been just one attempt to randomize patients to different treatment settings and, unfortunately, the comparison was compromised by the unsurprising finding that many patients randomized to in-patient treatment did not want it. In-patient treatment is used differently in different places; for example, it is common in some countries but unusual in others, and length of stay also varies markedly. Such differences are not evidence-based as in-patient treatment has received scant research attention. Even the most basic questions about in-patient treatment have not been adequately formulated, let alone addressed. For example, not only are the indications for hospitalization not established, but the specific goals are not agreed nor is it known how best to achieve them. Also, it is not clear whether the indications, goals and treatments should differ for adolescents and adults. At best, there is modest evidence from cohort studies to support a focus on eating and an emphasis on weight regain. Comparisons of flexible behavioral programs with more rigid ones have either yielded no significant differences in the rate of weight regain or have favored the more flexible regimes. There is no evidence that drug treatment significantly enhances weight regain. Even less is known about day patient treatment. Again, the indications are not agreed and the goals not established. It is not clear whether day patient treatment is best viewed as a less expensive alternative to in-patient treatment, as an intensive form of out-patient treatment, or as a distinct modality with particular strengths and weaknesses. Whatever the place of in-patient and day patient treatment, out-patient treatment is the mainstay of the treatment of anorexia nervosa. Out-patient treatment is the sole treatment for many patients, and even if patients receive in-patient or day patient treatment, it is usually followed by out-patient treatment. Turning to the form of treatment provided, there is no evidence to support the use of drugs in the treatment of anorexia nervosa. An initial report on young adults suggested that fluoxetine reduced the rate of relapse following in-patient treatment but a subsequent well-conducted two-center study, again on young adults, failed to replicate the finding (Walsh, Kaplan, Attia et al., 2006). Nor is there evidence to support any specific psychological treatment. It is widely thought that there is good evidence to support the use of family therapy to treat adolescents with the disorder. This is not the case. There have been two comparisons of family therapy with another form of treatment. In the first, Russell, Szmukler, Dare, & Eisler (1987) compared 1 year of an eating disorderfocused form of family therapy with 1 year of supportive psychotherapy in patients who had just been discharged from a specialist in-patient unit (mean age 16.6 years, mean duration of eating disorder 1.2 years). The family therapy studied has since come to be known as the “Maudsley method” (Lock, le Grange, Agras, & Dare, 2001). The results favored the family therapy, both at the end of treatment and 5 years later (Eisler, Dare, Russell et al., 1997; Russell, Szmukler, Dare et al., 1987). The first study involved a comparison of a treatment similar to the Maudsley method with a psychodynamically oriented treatment in which the adolescent patients were seen individually with occasional supportive sessions for their parents (Robin, Siegel, Moye et al., 1999). The outcome of both groups was good, both at the end of treatment and 1 year later. There was one statistically significant difference between them; in terms of increase in body mass index the patients in the family therapy condition did better. However, it is not possible to attribute this finding to the family therapy as many of the patients were hospitalized during their treatment and this was especially common among those who received family therapy. In summary, only two studies have compared family therapy with another form of treatment and the findings of the second are uninterpretable. Thus, the case for favoring family therapy over other forms of treatment rests on a single study (Russell, Szmukler, Dare et al., 1987) which involved just 21 patients – 10 of whom received family therapy – all of whom had recently been discharged from a specialist in-patient unit. This is a very modest body of data and one of questionable relevance to routine out-patient treatment. It must also be noted that the superiority of the family therapy over the supportive psychotherapy condition might not have been because of the involvement of the patient’s family because there was another important difference between the two treatments: the family therapy placed great emphasis on getting patients to eat well and maintain a healthy weight, whereas there was nothing like EATING DISORDERS 679 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 679

the same focus on eating and weight in the supportive psychotherapy condition. In addition to these two studies, there have been comparisons of different ways of administering the Maudsley method. Their findings are also inconclusive, in part because the studies have been small in size and therefore underpowered. Interestingly, there is no evidence that seeing the family together is superior to seeing them separately from the young person (Eisler, Dare, Hodes et al., 2000). There has also been a larger-scale comparison of a 6-month 10-session version of the treatment with a 12-month 20-session version (Lock, Agras, Bryson, & Kraemer, 2005). They were equally effective. Clearly, what are needed are adequately powered comparisons of the Maudsley method of family therapy with other forms of treatment, both individual and family-based. It is plausible that family therapy might best suit younger adolescents while a more individually focused form of treatment (such as cognitive–behavior therapy), but one nevertheless involving the family, might be a better option for older patients. Bulimia Nervosa There have been no studies of the treatment of adolescents with bulimia nervosa. However, there have been over 50 randomized controlled trials evaluating treatments for adults and the main findings are reasonably consistent (National Institute for Clinical Excellence, 2004). Although almost all the trials have been efficacy rather than effectiveness studies, there are good reasons to think that their findings are relevant to most psychiatric settings. Three main findings have emerged. First, the great majority of patients can be managed on an out-patient basis. Second, the most effective treatment is a specific type of cognitive–behavior therapy that focuses on modifying the behavior and ways of thinking that are thought to maintain these patients’ eating disorder (Fairburn, 2006; Fairburn, Marcus, & Wilson, 1993). The treatment typically involves about 20 individual treatment sessions over 5 months. The third finding is that antidepressant drugs have an “antibulimic” effect. They often result in a rapid decline in the frequency of binge eating and purging, and an improvement in mood, but meta-analysis indicates that the effect is not as great as that obtained with cognitive–behavior therapy (National Institute for Clinical Excellence, 2004) and, more importantly, clinical experience and the limited research evidence suggest that it is often not sustained (Walsh, Hadigan, Devlin, Gladis, & Roose, 1991). None of these data have come from studies of adolescents. Three less robust findings have also emerged. First, combining cognitive–behavior therapy with antidepressant drugs results in few consistent benefits over cognitive–behavior therapy alone. Second, data from two trials suggest that “interpersonal psychotherapy” (IPT), a well-known focal psychotherapy (Weissman, Markowitz, & Klerman, 2000), may be as effective as cognitive–behavior therapy but it takes considerably longer to work. Third, simple, largely behavioral treatments (including forms of self-help) that include elements of cognitive–behavior therapy may help a subset of patients although they are unlikely to be sufficient for the majority. In the absence of research focused on adolescents, the assumption is that cognitive–behavior therapy, suitably modified (Wilson & Sysko, 2006), is likely to be the most effective form of treatment. A possible alternative is interpersonal psychotherapy, an adolescent version of which exists (Mufson, Dorta, Moreau, & Weissman, 2004). For younger adolescents eating disorder-focused family therapy is the other obvious treatment option. Eating Disorder NOS There have been no studies of the treatment of eating disorder NOS, either in adults or adolescents. This is a remarkable omission given that this is the most common eating disorder diagnosis. Clinical Recommendations Assessment While the general principles of assessment in child and adolescent psychiatry apply to patients with eating disorders, it is worth emphasizing the importance of certain aspects of the assessment. Frequently, young people with eating disorders are at a developmental stage when they are negotiating independence from their parents. A significant proportion will be having difficulty with this developmental stage, either attempting to exert their independence and rule parents out of having a role in their lives or else behaving in an immature dependent fashion. It is generally helpful to take an approach that is respectful and age-appropriate but recognizes the role of parents in providing a developmental history, their perspective on the problem and their potential role in treatment. At the same time, whatever the age of the patient, it is important to acknowledge overtly their own perspective. Within any assessment, time should be set aside to enable a sympathetic understanding of the young person’s point of view and a full assessment of their mental state including cognition and risk. This can only be conducted with the young person alone. Thus, there needs to be an individual assessment in addition to a joint interview with the parents. Some advocate a separate parental interview but the gains in terms of information gathering may be offset by the alienation of the young person and potential breaches of confidentiality. Attention to the young person’s physical state is also important if there is a risk that it might be affected. Management of Anorexia Nervosa Effective management comprises interventions for both the psychological and physical aspects of the disorder. The relative importance of each will depend on the degree of physical ill health, but it is important to keep in mind that the physical features are merely consequences of the underlying illness and that restoration of physical health alone cannot be expected CHAPTER 41 680 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 680

EATING DISORDERS 681 to cure the disorder. When anorexia nervosa has been present for any length of time, adverse social and educational consequences generally follow and so a rehabilitative component will also need to be added to the treatment plan. The psychological features include specific abnormal cognitions related to weight and shape and, commonly, non-specific negative cognitions of ineffectiveness, low mood, guilt and worthlessness. Many young people also have regressed to an immature developmental stage in which they have relinquished ageappropriate responsibility and autonomy. Therefore there is a danger in addressing the physical aspects of the condition that steps by parents and clinicians to take behavioral control will exacerbate the psychological disturbance. Generally, treatment should be planned to span at least 6 months and only a minority will have fully recovered in 1 year. In other than the mildest cases, treatment should be offered by services experienced in the management of eating disorders. Two important early considerations are when to admit to hospital and the relative importance of family versus individual therapies. A distinction should be drawn between medical admission to address physical complications and psychiatric admission to treat the underlying disorder. The former is clearly indicated in situations of medical instability, when short-term pediatric management usually benefits from a degree of psychiatric liaison. Although lengthy psychiatric admission is offered in many countries other than the USA, combining psychological therapies with full weight restoration, evidence for the effectiveness of this very expensive approach is lacking. Education is an essential element of treatment. The young person and his or her parents need to be educated about eating disorders and their management. Often, efforts to give the young person an understanding of the disorder, particularly if the young person is seen alone, make it possible to effectively engage them as a patient. It is often useful if the clinician attempts to empathize with the young person’s experience and how it has led to the eating disorder. When outlining the treatment plan, it is important to highlight the role of the patient and generally the family in bringing about change. At one end of the spectrum, the parents’ role may be merely to support the young person and encourage their out-patient attendance. At the other extreme (as in the Maudsley method; Lock, le Grange, Agras et al., 2001), their involvement in meal production and supervision may be crucial. Obtaining the young person’s motivation and cooperation can be extremely difficult and it may be necessary to address this continually during treatment. An approach that aims to work with, rather than against the young person, empathizes with their predicament and fears, and instills hope that change will lead to benefits while acknowledging the costs, is generally most productive. In all but the mildest cases, a multidisciplinary approach is recommended. The treating team will usually comprise a psychiatrist, an individual psychotherapist (of whatever discipline), a family therapist, a physician and a nutritionist/dietitian. Specialist in-patient and day patient services may include a physiotherapist, occupational or creative therapists, and teachers. The management plan will vary for younger children and also for boys. Talking therapies must be age-appropriate and will often use art and other non-verbal approaches with younger patients. Parents of younger children will have a greater role in supporting treatment, particularly in meal planning and supervised eating. In older adolescents, recovery generally implies restoration to a premorbid state of physical health (i.e., return of weight and hormonal functioning against a background of completed growth). In pubescent girls, treatmentimposed weight gain may precipitate the menarche, with all that that implies experientially. A recovering prepubertal child will face the uncertainty of a physical and social identity that has not been experienced before. In a number of respects this will mean “growing up,” and addressing the attendant anxieties that may have played a part in the original development of the condition. A related issue concerns the need to ensure that the “recovered” child or adolescent does not “stand still” – that is to say a 13-year-old restored to a healthy weight might be considered recovered but their health will decline if they are unable to keep pace with the expected trajectories of healthy physical and social development. The presentation and management of boys are essentially similar to those of girls. However, boys will be expected to continue growth into their late teenage years and ongoing supervision should ensure that their growth potential is maintained. Some boys are uncertain about their sexual identity and such anxieties may be exacerbated by attending a service that predominantly caters for girls. Services should include staff who are familiar with, and comfortable discussing, the common developmental concerns of pubertal boys. Physical Management Because of the potentially irreversible effect of anorexia nervosa on adolescent growth and development, the threshold for medical intervention should be lower in children and adolescents than adults. Furthermore, medical complications can occur early in younger subjects before evidence of significant weight loss. Prepubertal children are at particular risk of physical complications of starvation because of their relative lack of body fat and a tendency to dehydrate quickly. Routine blood count, electrolyte levels and liver and thyroid function should be measured. Assessment of serum calcium, phosphate, vitamin B12 and folate is indicated in severe starvation and during refeeding. Height and weight should be plotted on centile charts and if possible related to premorbid values. Heart rate and blood pressure should be measured and an electrocardiogram performed if cardiac function is compromised or antidepressant treatment proposed. Pubertal status may be assessed by Tanner staging, which provides mean ages and ranges for the development of secondary sexual characteristics. Concerns arise if this staging is more than two standard deviations behind the mean. Ultrasonography can confirm (and enable monitoring 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 681

CHAPTER 41 682 of) ovarian function, although an overemphasis on physical progress should be avoided. When treating the malnourished young person, care should be taken to avoid the refeeding syndrome, a potentially lifethreatening disturbance of fluid and electrolyte balance which can follow sudden increases in nutritional intake in those who have been in a state of starvation. This can be achieved by regular monitoring of heart rate, orthostatic vital signs and serum electrolytes including phosphorus, glucose, magnesium and potassium, although total body electrolytes may be depleted even in the presence of normal serum levels. Note that the refeeding syndrome occurs more commonly with parenteral than enteral feeding. There is a lack of consensus regarding oral feeding requirements. A weight gain of around 1 kg per week is generally recommended for in-patients and 0.5 kg per week for out-patients. After an initial safe weight has been achieved, the young person’s food intake should be adjusted to ensure that growth is in keeping with normal weight and height trajectories. Weight restoration should utilize the least invasive procedures possible and should be provided within a caring ageappropriate setting. Nasogastric feeding should only be resorted to in the face of persistent refusal to eat normally. Strict behavioral regimes in which young people have to earn privileges through eating and weight gain are not desirable or acceptable as they militate against the therapeutic alliance and there is no evidence that these approaches work, other than by achieving short-term weight gain. In the long term, undue coercion either may be perceived by the young person as a recapitulation of abuse or neglect that they may have suffered previously or it may reinforce low self-esteem and feelings of ineffectiveness, both of which are common antecedents of anorexia nervosa. Psychological Treatment All young people should have individual psychological therapies to address their specific and non-specific psychopathology. Such features as clinical perfectionism, mood disorder and peer relationship difficulties can usefully be addressed. The behavioral aspects of treatment should also be tackled, hence a cognitive–behavioral approach rather than a supportive or insight-orientated one is to be preferred. The practical aspects of treatment are often ineffective unless the parents are also involved in establishing behavioral control. Parental responsibility for the behavioral aspects of treatment (e.g., dietary planning, involvement in sports), should be age-appropriate and therefore greater with younger patients. Family interventions may also be useful in tackling family communication and relationship problems but it should be noted that the outcomes of family interventions for families with high expressed emotion have to date been poor. Pharmacological Treatment There is no evidence to support the use of medication in the treatment of eating disorders. Medication may be indicated to treat comorbid disorders, especially depression and obsessivecompulsive disorder. Depressive symptoms are a feature of starvation and so are common in anorexia nervosa. This said, there is a subgroup of adult patients who have a true comorbid clinical depression as indicated by a broad range of depressive features (e.g., hopelessness, thoughts of death and dying, pathological guilt, decreased energy and drive). With such patients, antidepressant medication is indicated. In adolescents in whom “biological” symptoms are less common, the role of antidepressants is less clear and major concerns exist about unwanted effects. Fluoxetine is currently the only antidepressant recommended for first-line use in adolescents in most countries and is sometimes used on empirical grounds. Minor tranquillizers are sometimes used symptomatically to reduce high levels of anxiety, particularly around eating. Management of Bulimia Nervosa As in the treatment of anorexia nervosa, treatment should include motivational aspects, attention to physical complications, and cognitive and behavioral elements. Young people may benefit from their parents’ involvement, both to assist in meal planning and other practical issues, and also to enable parents to better understand the condition and the treatment plan. As young people rarely present with bulimia nervosa before 16 years of age, the involvement of parents will usually be at the young person’s discretion. Psychological Treatment Although there have been no adequate studies of psychological treatments for adolescents with bulimia nervosa, it seems appropriate to offer them the empirically supported treatments developed for adults, specifically cognitive–behavior therapy, with appropriate modifications for adolescents (Wilson & Sysko, 2006). The main modifications are the use of ageappropriate written material, the involvement of the family (chiefly the parents), and the addressing of the developmental challenges faced by this age group (e.g., peer relationships, education, use of alcohol, rebellion and conformity). Parents may benefit from psychoeducation delivered either face-to-face, through reading material or by attending a parental support group. Group parental meetings are particularly helpful when the young person declines to involve the parents in their treatment. Pharmacological Treatment Arguably, this is not indicated because the research on adults indicates that the beneficial effects are less than those obtained with cognitive–behavior therapy and they tend not to be maintained. They could be used as an initial step in management. Recent findings suggest that if patients do not show an early response (within 2 weeks), they are unlikely to benefit (Walsh, Kaplan, Attia et al., 2006). Physical Management The main physical complications of bulimia nervosa are disturbances of fluid and electrolyte balance resulting from vomiting and laxative misuse. Hypokalemia should be treated with 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 682

oral potassium supplements. Advice on dental hygiene should be offered to avoid the effects of acid erosion. Psychiatric admission to hospital is not recommended, but on rare occasions medical admission may be required to correct physical complications (e.g., when bulimia nervosa coexists with diabetes mellitus). Management of Eating Disorder NOS The UK NICE guidelines addressed the absence of any research on the treatment of eating disorder NOS by recommending that clinicians follow bulimia nervosa treatment guidelines with cases resembling bulimia nervosa and anorexia nervosa guidelines with cases resembling anorexia nervosa (National Institute for Clinical Excellence, 2004). The trouble with this recommendation is that most cases within eating disorder NOS are of the “mixed” variety rather than subthreshold forms of anorexia nervosa or bulimia nervosa. Of relevance to this gap in knowledge is the development of a new “transdiagnostic” form of cognitive–behavior therapy designed to be suitable for the full range of clinical eating disorders seen in clinical practice including eating disorder NOS (Fairburn, 2006; Fairburn, Cooper, & Shafran, 2003). Emerging evidence suggests that it is as effective as a treatment for eating disorder NOS as it is for bulimia nervosa. This treatment is beginning to be used with adolescents incorporating modifications of the type outlined above. Ethical and Legal Issues Eating disorders are unusual amongst presentations in Child and Adolescent Psychiatry in that they are potentially lifethreatening and may have very serious physical and psychosocial consequences if effective treatment is not provided. Given that young people with eating disorders are often reluctant to seek or accept treatment, practitioners need effective ethical and legal guidelines in order to make treatment decisions (Foreman, 2006). Where at all possible attempts should be made to establish a therapeutic alliance with the young person, both in order to achieve consent to treatment on ethical grounds and also because effectiveness of treatment depends in large part on the patient’s cooperation. In the former case, many countries permit parents or those with parental authority to consent to treatment on their child’s behalf even in the face of the child’s opposition. In England and Wales, parents may consent on their children’s behalf up to the age of 18 but different countries operate different age limits. In considering the desirability of obtaining the young person’s consent, a distinction should be drawn between treatment directed at reducing risk from the physical consequences of the eating disorder and treatment of the disorder itself. Physical aspects of treatment (e.g., refeeding) may be provided in extreme situations without the young person’s consent and may on occasion be life-saving. However, the psychological and behavioral aspects of the disorder require psychological interventions. While family interventions can proceed to some extent without the young person’s agreement, individual psychotherapy requires the active participation of the patient if it is to be effective. On occasion young people with anorexia nervosa decline treatment and clinicians have to decide whether to proceed with treatment against the patient’s will. Rarely, similar considerations apply to extreme cases of bulimia nervosa (e.g., when it is combined with diabetes mellitus). In general, the decision surrounds the desirability of admission to hospital. Given the relatively poor outcome of in-patient treatment for anorexia nervosa in terms of producing full and lasting recovery and the probable poorer outcome in those opposed to treatment, this step should probably only be taken in cases where the child is in acute medical danger. In the UK, there are three potential approaches to the compulsory treatment of young people under the age of 18: 1 Treatment on the basis of parental consent; 2 Treatment under the Mental Health Act (1983); and 3 Treatment under the Children Act (1989; see chapter 8). Legislation differs between countries but a number of principles underlying the choice apply. Parental consent is often the appropriate framework to employ, particularly in younger patients and in the short term. In many cases, the young person’s opposition will diminish in the early days of an admission once attempts have been made to engage them and they feel safe within the treatment setting. Nevertheless, in these cases the young person’s lack of initial agreement to treatment should be recorded, along with the legal basis for proceeding. Where the young person’s opposition is not readily overcome, is persistent, leads to absconding or requires active treatment against his or her wishes (e.g., nasogastric feeding), consideration should be given to using mental health legislation to provide the basis for treatment. Prevention of Eating Disorders From conceptual and methodological points of view there are many difficulties to overcome when considering how to develop and test means of preventing eating disorders (Commission on Adolescent Eating Disorders, 2005; Piran, Levine, & Steiner-Adair, 1999). First, there are no substantiated modifiable risk factors. As a result there are no clear targets for preventive interventions. Second, eating disorders are uncommon, with the consequence that to demonstrate that an intervention was effective would require a study on a huge scale. To get round this problem researchers have focused on modifying dieting and concerns about shape and weight. The trouble with this strategy is that these phenomena, while of interest and possible concern, have only a loose relationship to eating disorders of clinical severity. The studies themselves have had other shortcomings. Sample sizes have been relatively small, assessment measures weak and follow-up periods short. As a result of these and other problems, little is known. The interventions tested so far have mostly been “universal” interventions rather than “targeted” ones, and they have generally taken place in schools. To an extent some have had EATING DISORDERS 683 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 683

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E., Meltzer, C. C., Price, J. C., et al. (2005). Serotonin alterations in anorexia and bulimia nervosa: New insights from imaging studies. Physiology & Behavior, 85, 73–81. Kaye, W. H., Wagner, A., Frank, G., & Bailer, U. F. (2006). Review of brain imaging in anorexia and bulimia nervosa. In S. Wonderlich, J. E. Mitchel, M. de Zwaan, & H. Steiger (Eds.), Annual review of eating disorders, Part 2 (pp. 113–129). Oxford: Radcliffe. Keel, P. K., Mitchell, J. E., Miller, K. B., Davis, T. L., & Crow, S. J. (1999). Long-term outcome of bulimia nervosa. Archives of General Psychiatry, 56, 63–69. Keel, P. K., Dorer, D. J., Eddy, K. T., Franko, D., Charatan, D. L., & Herzog, D. B. (2003). Predictors of mortality in eating disorders. Archives of General Psychiatry, 60, 179–183. Keel, P. K., & Klump, K. L. (2003). Are eating disorders culture-bound syndromes? Implications for conceptualizing their etiology. Psychological Bulletin, 129, 747–769. Key, A., Mason, H., & Bolton, J. (2000). 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CHAPTER 41 684 limited success in that they have increased knowledge about eating disorders and healthy weight regulation, but few have altered attitudes or actual behavior even in the short term. An unmet challenge is how to integrate eating disorder-focused preventive interventions – which generally aim to reduce dieting and concerns about shape and weight – with those targeted at the prevention of obesity, a more pressing health problem. Acknowledgments CGF is supported by a Principal Research Fellowship (046386) from the Wellcome Trust. References Arsenault, L., Moffitt, T. E., Caspi, A., Taylor, P. J., Silva, P. A. (2000). Mental disorders and violence in a total birth cohort: Results from the Dunedin Study. Archives of General Psychiatry, 57, 979–986. Becker, A. E., & Fay, K. (2006). Sociocultural issues and eating disorders. In S. Wonderlich, J. E. Mitchell, M. de Zwaan, & H. Steiger (Eds.), Annual review of eating disorders, Part 2 (pp. 35–63). Oxford: Radcliffe. 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Stein, A., Woolley, H., Murray, L., et al. (2001). Influence of psychiatric disorder on the controlling behaviour of mothers with 1- year-old infants. A study of women with maternal eating disorder, post-natal depression and a healthy comparison group. British Journal of Psychiatry, 179, 157–162. Steinhausen, H-C. (2002). The outcome of anorexia nervosa in the twentieth century. American Journal of Psychiatry, 159, 1284– 1293. Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2000). Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. American Journal of Psychiatry, 157, 393–401. Strober, M., Freeman, R., & Morrell, W. (1997). The long-term course of severe anorexia nervosa in adolescents: Survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study. International Journal of Eating Disorders, 22, 339–360. van Son, G. E., van Hoeken, D., Bartelds, A. I. M., van Furth, E. F., & Hoek, H. W. (2006). Time trends in the incidence of eating disorders: A primary care study in the Netherlands. International Journal of Eating Disorders, 39, 565–569. Walsh, B. T., Hadigan, C. M., Devlin, M. J., Gladis, M., & Roose, S. P. (1991). Long-term outcome of antidepressant treatments for bulimia nervosa. American Journal of Psychiatry, 148, 1206– 1212. Walsh, B. T., Kaplan, A. S., Attia, E., Olmsted, M., Parides, M., Carter, J. C., et al. (2006). Fluoxetine after weight restoration in anorexia nervosa: A randomized controlled trial. Journal of the American Medical Association, 295, 2605–2612. Weissman, M. M., Markowitz, J. C., & Klerman, G. L. (2000). Comprehensive guide to interpersonal psychotherapy. New York: Basic Books. Wilson, G. T., & Sysko, R. (2006). Cognitive–behavioural therapy for adolescents with bulimia nervosa. European Eating Disorders Review, 14, 8–16. Zipfel, S., Lowe, B., & Herzog, W. (2003). Medical complications. In J. Treasure, U. Schmidt, & E. Van Furth (Eds.), Handbook of eating disorders (2nd edn., pp. 169–90). Chichester: Wiley. EATING DISORDERS 685 Lock, J., le Grange, D., Agras, W. S., & Dare, C. (2001). Treatment manual for anorexia nervosa: A family-based approach. New York: Guilford Press. Mufson, L., Dorta, K. P., Moreau, D., & Weissman, M. M. (2004). Interpersonal psychotherapy for depressed adolescents (2nd edn.) New York: Guilford Press. National Institute for Clinical Excellence. (2004). Eating disorders: Core interventions in the treatment and management of eating disorders in primary and secondary care. London: National Institute for Clinical Excellence. Nicholls, D., Chater, R., & Lask, B. (2000). Children into DSM don’t go: A comparison of classification systems for eating disorders in childhood and early adolescence. International Journal of Eating Disorders, 28, 317–324. Piran, N., Levine, M. P., & Steiner-Adair, C. (1999). Preventing eating disorders. New York: Brunner/Mazel. Råstam, M., Gillberg, C., & Wentz, E. (2003). Outcome of teenageonset anorexia nervosa in a Swedish community-based sample. European Child and Adolescent Psychiatry, 12, 78–90. Robin, A. L., Siegel, P. T., Moye, A. W., Gilroy, M., Dennis, A. B., & Sikand, A. (1999). A controlled comparison of family versus individual therapy for adolescents with anorexia nervosa. Journal of the American Academy of Child and Adolescent Psychiatry, 38, 1482–1489. Russell, G. F. M. (1992). Anorexia nervosa of early onset and its impact on puberty. In P. Cooper (Ed.), Feeding problems and eating disorders in children and adolescents (pp. 85–112). Chur: Harwood Academic. Russell, G. F. M., Szmukler, G. I., Dare, C., & Eisler, I. (1987). An evaluation of family therapy in anorexia nervosa and bulimia nervosa. Archives of General Psychiatry, 44, 1047–1056. Silva, P. A., & Stanton, W. R. (1997). From Child to Adult: The Dunnedin Multidisciplinary Health and Development Study. New York, NY: Oxford University Press. Slof-Op ‘t Landt, M., van Furth, E. F., Meulenbelt, I., Slagboom, R. E., Bartels, M., Boomsma, D. I., et al. (2005). Eating disorders: From twin studies to candidate genes and beyond. Twin Research and Human Genetics, 8, 467–482. 9781405145497_4_041.qxd 29/03/2008 02:53 PM Page 685

686 Both ICD-10 (WHO, 1996) and DSM-IV (APA, 2000) diagnostic systems now acknowledge that major stressors can cause serious morbidity and that children may suffer from posttraumatic stress disorder (PTSD). The past 15 years have seen a great increase in studies of the effects of major stresses, as encountered in disasters, war and other life-threatening experiences. However, the question for child psychiatry remains whether severe acute stresses (see chapter 26), as opposed to chronic ones linked to social adversity (see chapter 25), carry a substantial increased risk of psychiatric sequelae. If so, what sort of stressors carry such increased risk? What are the most common psychological sequelae? Do these vary according to stressor, according to developmental level? What is the role of the family in moderating the reactions? Are there other known risk and protective factors? Indeed, is PTSD a truly separate disorder or is it merely a variant of other wellrecognized disorders such as anxiety, phobias and depression? Finally, what is currently known about intervention? Concept of Post-Traumatic Stress Disorder The diagnosis of PTSD was first conceptualized in response to observations of Vietnam war veterans presenting with what came to be recognized as a particular pattern of symptoms in three clusters: intrusive recollections of a traumatic event; emotional numbing and avoidance of reminders of that event; and physiological hyperarousal. In retrospect, similar patterns were noted as reactions in earlier wars and in prospect, the criteria were adapted, partly operationalized and applied to adult civilians. Next, the diagnosis was applied to children who had experienced an “event outside the range of usual human experience . . . that would be markedly distressing to almost anyone” (DSM-III-R, 1987). Thus, it was argued that there were certain types of stressful experiences that were very severe and/or unusual and that there was a distinctive form of stress reaction to these. PTSD was classified as an anxiety disorder, but many argued that it should be included as a dissociative disorder. It was increasingly described as “a normal reaction to an abnormal situation,” and so, logically, it was queried whether it should be regarded as a psychiatric disorder at all (O’Donohue & Eliot, 1992). Even if it were regarded as a normal reaction, it causes substantial impairment in sufficient cases to be regarded as a disorder. Results from studies of adults have reasonably established that PTSD, while being predominantly an anxiety disorder, differs from other anxiety disorders in important ways. Thus, Foa, Steketee, & Olasov-Rothbaum (1989) showed that the trauma suffered violated more of the patient’s safety assumptions than did events giving rise to other forms of anxiety. There was a much greater generalization of fear responses in the PTSD groups, and, unlike other anxious patients, they reported far more frequent re-experiencing of the traumatic event. Indeed, it is this internal, subjective experience that seems most to mark out PTSD from other disorders (Jones & Barlow, 1992). Epidemiological investigations in adults suggest that exposure to traumatic events is common (Kessler, Sonnega, Bromet et al., 1995), and that only a minority of exposed individuals go on to develop the disorder (McFarlane, 2005). The argument is therefore made that PTSD is an “abnormal reaction” that involves a complex interaction of biological, psychological and social causes (Yehuda & McFarlane, 1995); exposure to trauma is insufficient to explain development of the disorder. Current biopsychosocial and cognitive models (see p. 689) are paying increasing attention to factors underlying individual differences in response to traumatic events. Concern has been expressed that there are other forms of stress reactions to chronic stressors as experienced in repeated physical or sexual abuse (see chapters 28 and 29). Terr (1991), for example, draws a distinction between type I and II traumas, roughly the distinction between acute and chronic. While these are important debates that will alter the views taken on PTSD, here we concentrate on acute conditions as manifested in children and adolescents. With its roots in studies of adult psychopathology, the concept has been uneasily extended to apply to stress reactions in children and adolescents. The major difficulty from the outset has been that some of the symptoms are developmentally inappropriate for younger people. Indeed, the younger the child, the less appropriate the criteria. Many writers agree that it is very difficult to elicit evidence of emotional numbing in children (Frederick, 1985). Some children do show loss of interest in activities and hobbies that previously gave them pleasure. Preschool children show much more regressive behavior as Post-Traumatic Stress Disorder 42 William Yule and Patrick Smith 9781405145497_4_042.qxd 29/03/2008 02:53 PM Page 686 Rutter’s Child and Adolescent Psychiatry, 5th Edition, Edited by M. Rutter, D. V. M. Bishop D. S. Pine, S. Scott, J. Stevenson, E. Taylor and A. Thapar © 2008 Blackwell Publishing Limited. ISBN: 978-1-405-14549-7