Employers such as the Armed Forces (AF) and emergency services, who predictably expose their staff to potentially traumatic events (PTEs), often provide psycho-educational briefings in an attempt to mitigate possible adverse psychological sequelae. Within the military, psycho-educational briefings are widely used, particularly following exposure to PTEs on operations. The aim of this review was to evaluate the efficacy of these interventions and make appropriate recommendations.

A search of Medline, PsycINFO and EMBASE was conducted, bibliographies of retrieved articles were searched and experts in the field were consulted.

Two surveys and seven intervention studies were identified for inclusion in the review. Only three studies were randomized controlled trials (RCTs). Overall, the review found some evidence of benefit of psycho-educational interventions but it was not consistent across studies or outcomes and effects were small. However, there was also little evidence to suggest that they caused harm. There was some evidence that the beneficial effects may be greater for those who have been exposed to a higher number of PTEs.

Given the high operational tempo currently faced by coalition forces personnel, there remains a pressing need to identify the most effective way of minimizing the impact of exposure to potentially traumatic deployment incidents. To date, few psycho-educational interventions designed to prevent deployment-related psychological ill-health have been evaluated systematically in methodologically robust studies. The review recommends that future interventions are theoretically based and evaluated in cluster RCTs that examine both process and outcome variables.

National Guard troops are at increased risk for post-traumatic stress disorder (PTSD); however, little is known about risk and resilience in this population.

The Readiness and Resilience in National Guard Soldiers Study is a prospective, longitudinal investigation of 522 Army National Guard troops deployed to Iraq from March 2006 to July 2007. Participants completed measures of PTSD symptoms and potential risk/protective factors 1 month before deployment. Of these, 81% (n=424) completed measures of PTSD, deployment stressor exposure and post-deployment outcomes 2–3 months after returning from Iraq. New onset of probable PTSD ‘diagnosis’ was measured by the PTSD Checklist – Military (PCL-M). Independent predictors of new-onset probable PTSD were identified using hierarchical logistic regression analyses.

At baseline prior to deployment, 3.7% had probable PTSD. Among soldiers without PTSD symptoms at baseline, 13.8% reported post-deployment new-onset probable PTSD. Hierarchical logistic regression adjusted for gender, age, race/ethnicity and military rank showed that reporting more stressors prior to deployment predicted new-onset probable PTSD [odds ratio (OR) 2.20] as did feeling less prepared for deployment (OR 0.58). After accounting for pre-deployment factors, new-onset probable PTSD was predicted by exposure to combat (OR 2.19) and to combat's aftermath (OR 1.62). Reporting more stressful life events after deployment (OR 1.96) was associated with increased odds of new-onset probable PTSD, while post-deployment social support (OR 0.31) was a significant protective factor in the etiology of PTSD.

Combat exposure may be unavoidable in military service members, but other vulnerability and protective factors also predict PTSD and could be targets for prevention strategies.

Acute stress disorder involves prominent symptoms of threat avoidance. Preliminary cross-sectional data suggest that such threat-avoidance symptoms may also manifest cognitively, as attentional threat avoidance. Confirming these findings in a longitudinal study might provide insights on risk prediction and anxiety prevention in traumatic exposures.

Attention-threat bias and post-traumatic symptoms were assessed in soldiers at two points in time: early in basic training and 23 weeks later, during advanced combat training. Based on random assignment, the timing of the repeat assessment occurred in one of two schedules: for a combat simulation group, the repeat assessment occurred immediately following a battlefield simulation exercise, and for a control group, the assessment occurred shortly before this exercise.

Both groups showed no threat-related attention bias at initial assessments. Following acute stress, the combat simulation group exhibited a shift in attention away from threat whereas the control group showed no change in attention bias. Stronger threat avoidance in the combat simulation group correlated with severity of post-traumatic symptoms. Such an association was not found in the control group.

Acute stress may lead some individuals to shift their attention away from threats, perhaps to minimize stress exposure. This acute attention response may come at a psychological cost, given that it correlates with post-traumatic stress disorder (PTSD) symptoms. Further research is needed to determine how these associations relate to full-blown PTSD in soldier and civilian populations.

Evidence is accumulating that child sexual abuse (CSA) is associated with many psychiatric disorders in adulthood. This paper uses the detailed information available from the 2007 Adult Psychiatric Morbidity Survey of England (APMS 2007) to quantify links between CSA and a range of psychiatric conditions.

The prevalence of psychiatric disorder was established in a random sample of the English household population (n=7403), which also provided sociodemographic and experiential information.

We analyzed six types of common mental disorder, alcohol abuse and drug abuse, and people who screened positively for post-traumatic stress disorder (PTSD) and eating disorders. All were strongly and highly significantly associated with CSA, particularly if non-consensual sexual intercourse was involved, for which odds ratios (ORs) ranged from 3.7 to 12.1. These disorders were also related to adult sexual abuse (ASA), although the likelihood of reverse causality is then increased. Revictimization in adulthood was common, and increased the association of CSA with disorder. For several disorders, the relative odds were higher in females but formal tests for moderation by gender were significant only for common mental disorders and only in relation to non-consensual sexual intercourse. The population attributable fraction (PAF) was higher in females in all cases.

The detailed and high-quality data in APMS 2007 provided important confirmation both of the strength of association of CSA with psychiatric disorder and of its relative non-specificity. Our results have major implications at the public health level and the individual level, in particular the need for better recognition and treatment of the sequelae of CSA.

Prior work has suggested that genetic influences on major depressive disorder (MDD) may be activated by the experience of negative life events. However, it is unclear whether these results persist when controlling for the possibility of confounding active gene–environment correlations (rGE).

We examined a sample of 1230 adopted and biological siblings between the ages of 10 and 20 years from the Sibling Interaction and Behavior Study. MDD was measured via a lifetime DSM-IV symptom count. Number of deaths experienced served as our environmental risk experience. Because this variable is largely independent of the individual's choices/behaviors, we were able to examine gene–environment interactions while circumventing possible rGE confounds.

Biometric analyses revealed pronounced linear increases in the magnitude of genetic influences on symptoms of MDD with the number of deaths experienced, such that genetic influences were estimated to be near-zero for those who had experienced no deaths but were quite large in those who had experienced two or more deaths (i.e. accounting for roughly two-thirds of the phenotypic variance). By contrast, shared and non-shared environmental influences on symptoms of MDD were not meaningfully moderated by the number of deaths experienced.

Such results constructively replicate prior findings of genetic moderation of depressive symptoms by negative life events, thereby suggesting that this effect is not a function of active rGE confounds. Our findings are thus consistent with the notion that exposure to specific negative life events may serve to activate genetic risk for depression during adolescence.

We examined the different trajectories of vital exhaustion (VE) over a 12-month period and their impact on prognosis in a sample of myocardial infarction (MI) and chronic heart failure (CHF) patients.

Consecutive MI (n=407) and CHF patients (n=297) were assessed at baseline, and at 3- and 12-month follow-up for symptoms of VE. Latent growth mixture modelling was used to examine the course of VE over time. The combined clinical endpoint was defined as cardiac hospital readmission or death.

Four distinct trajectories for VE were found: low VE, decreasing VE, increasing VE, and severe VE. Sex, marital status, left ventricular ejection fraction, psychotropic medication, sample group (CHF v. MI) and depressive symptoms were associated with VE, varying according to classes. The mean follow-up period was 25.3 months in which 34.7% of the patients experienced an event. Multivariate Cox regression showed that, compared with patients in the low VE class, patients in the increasing VE class [hazard ratio (HR)=1.16, 95% confidence interval (CI) 1.58–3.61, p=0.01], and the severe VE class (HR=1.69, 95% CI 1.31–2.64, p=0.02) had an increased risk for adverse cardiovascular events (i.e. cardiovascular hospital readmission or cardiovascular death). Decreasing VE was not related to adverse cardiovascular events (HR=0.97, 95% CI 0.66–1.69, p=0.81).

VE trajectories varied across cardiac patients, and had a differential effect on cardiovascular outcome. Increasing VE and severe VE classes were predictors of poor cardiovascular prognosis. These results suggest that identification of cardiac patients with an increased risk of adverse health outcomes should be based on multiple assessments of VE.

To test whether receiving care from a health visitor (HV) trained in identification and psychological intervention methods prevents depression 6–18 months postnatally in women who are not depressed 6 weeks postnatally.

The study was a prospective cluster trial, randomized by GP practice, with follow-up for 18 months in 101 primary care teams in the Trent area of England. The participants were women scoring <12 on the postal Edinburgh Postnatal Depression Scale (EPDS) at 6 weeks postnatally (1474 intervention and 767 control women). Intervention HVs (n=89, 63 clusters) were trained in identifying depressive symptoms using the EPDS and face-to-face clinical assessment and in providing psychologically orientated sessions based on cognitive behavioral or person-centered principles. The control group comprised HVs (n=49, 37 clusters) providing care as usual (CAU). The primary outcome measure was the proportion of women scoring ⩾12 on the EPDS at 6 months postnatally. Secondary outcomes were mean EPDS score, Clinical Outcomes in Routine Evaluation – Outcome Measure (CORE-OM) score, State–Trait Anxiety Inventory (STAI), 12-item Short Form Health Survey (SF-12) and Parenting Stress Index Short Form (PSI-SF) scores at 6, 12 and 18 months.

After adjusting for individual-level covariates, living alone, previous postnatal depression (PND), the presence of one or more adverse life events and the 6-week EPDS score, the odds ratio (OR) for EPDS ⩾12 at 6 months was 0.71 [95% confidence interval (CI) 0.53–0.97, p=0.031] for the intervention group (IG) women compared with the control (CAU) group women. Two subgroups were formed by baseline severity: a ‘subthreshold’ subgroup with a 6-week EPDS score of 6–11 (n=999) and a ‘lowest severity’ subgroup with a 6-week EPDS score of 0–5 (n=1242). There was no difference in psychological effectiveness by subgroup (interaction term: z=−0.28, p=0.782).

This study provides new evidence of a universal, enduring preventive effect for depression in women who screen negative for depression postnatally.

Parental characteristics influence the risk of offspring suicide. In this study we wanted to separate the hereditary from the environmental influence of such factors by comparing their effects in the adopted versus non-adopted.

A register study was conducted in a national cohort of 2 471 496 individuals born between 1946 and 1968, including 27 600 national adoptees, followed-up for suicide during 1987–2001. Cox regression was used to calculate hazard ratios (HR) for suicide of socio-economic indicators of the childhood household and biological parents' suicide, alcohol abuse and psychiatric morbidity separately in the adopted and non-adopted. Differences in effects were tested in interaction analyses.

Suicide and indicators of severe psychiatric disorder in the biological parents had similar effects on offspring suicide in the non-adopted and adopted (HR 1.5–2.3). Biological parents' alcohol abuse was a risk factor for suicide in the non-adopted group only (HR 1.8 v. 0.8, interaction effect: p=0.03). The effects of childhood household socio-economic factors on suicide were similar in adopted and non-adopted individuals, with growing up in a single parent household [HR 1.5 (95% confidence interval 1.4–1.5)] as the most important socio-economic risk factor for the non-adopted.

The main familial effects of parental suicide and psychiatric morbidity on offspring suicide are not mediated by the post-natal environment or imitation, in contrast to effects of parental alcohol abuse that are primarily mediated by the post-natal environment. Social drift over generations because of psychiatric disorders does not seem likely to explain the association of socio-economic living conditions in childhood to suicide.

Longitudinal research supports that suicidal thoughts and behaviors in adolescence predict maladjustment in young adulthood. Prior research supports links between suicide attempt and aggression, perhaps because of a propensity for impulsive behavior in states of high negative affect that underlies both problems. Such vulnerability may increase risk for intimate partner violence and generally poor young adulthood relational adjustment.

A total of 153 men participated in annual assessments from ages 10–32 years and with a romantic partner at three assessments from ages 18–25 years. Multi-method/multi-informant constructs were formed for parent/family risk factors, adolescent psychopathology (e.g. suicide-attempt history, mother-, father-, teacher- and self-reported physical aggression) and young adulthood relational distress (jealousy and low relationship satisfaction) and maladaptive relationship behavior (observed, self- and partner-reported physical and psychological aggression toward a partner, partner-reported injury, official domestic violence arrest records and relationship instability).

Across informants, adolescent aggression was correlated with suicide-attempt history. With few exceptions, aggression and a suicide attempt in adolescence each predicted negative romantic relationship outcomes after controlling for measured confounds. Adolescent aggression predicted young adulthood aggression toward a partner, in part, via relationship dissatisfaction.

Boys' aggression and suicide-attempt history in adolescence each predict poor relationship outcomes, including partner violence, in young adulthood. Findings are consistent with the theory of a trait-like vulnerability, such as impulsive aggression, that undermines adaptation across multiple domains in adolescence and young adulthood. Prevention and intervention approaches can target common causes of diverse public health problems.

Personal debt is one of many factors associated with anxiety, depression and suicidality. The aim of this study was to examine the relationship between personal debt and suicidal ideation in the context of sociodemographic factors, employment and income, lifestyle behaviours, and recently experienced traumatic events.

Interviews were conducted with a random probability sample comprising 7461 respondents for the third national survey of psychiatric morbidity of adults in England. Fieldwork was carried out throughout 2007. The prevalence of suicidal thoughts in the past week, past year and lifetime was assessed and current sources of debt were recorded.

In 2007, 4.3% of adults in England had thought about taking their own life in the past 12 months, ranging from 1.8% of men aged ⩾55 years to 7.0% of women aged 35–54 years. Those in debt were twice as likely to think about suicide after controlling for sociodemographic, economic, social and lifestyle factors. Difficulty in making hire purchase or mail order repayments and paying off credit card debt, in addition to housing-related debt (rent and mortgage arrears), was strongly associated with suicidal thoughts. Feelings of hopelessness partially mediated the relationship between debt and suicidal ideation.

The number of debts, source of the debt and reasons for debt are key correlates of suicidal ideation. Individuals experiencing difficulties in repaying their debts because they are unemployed or have had a relationship breakdown or have heavy caring responsibilities may require psychiatric evaluation in addition to debt counselling.

The Met allele of the catechol-O-methyltransferase (COMT) valine-to-methionine (Val158Met) polymorphism is known to affect dopamine-dependent affective regulation within amygdala–prefrontal cortical (PFC) networks. It is also thought to increase the risk of a number of disorders characterized by affective morbidity including bipolar disorder (BD), major depressive disorder (MDD) and anxiety disorders. The disease risk conferred is small, suggesting that this polymorphism represents a modifier locus. Therefore our aim was to investigate how the COMT Val158Met may contribute to phenotypic variation in clinical diagnosis using sad facial affect processing as a probe for its neural action.

We employed functional magnetic resonance imaging to measure activation in the amygdala, ventromedial PFC (vmPFC) and ventrolateral PFC (vlPFC) during sad facial affect processing in family members with BD (n=40), MDD and anxiety disorders (n=22) or no psychiatric diagnosis (n=25) and 50 healthy controls.

Irrespective of clinical phenotype, the Val158 allele was associated with greater amygdala activation and the Met158 allele with greater signal change in the vmPFC and vlPFC. Signal changes in the amygdala and vmPFC were not associated with disease expression. However, in the right vlPFC the Met158 allele was associated with greater activation in all family members with affective morbidity compared with relatives without a psychiatric diagnosis and healthy controls.

Our results suggest that the COMT Val158Met polymorphism has a pleiotropic effect within the neural networks subserving emotional processing. Furthermore the Met158 allele further reduces cortical efficiency in the vlPFC in individuals with affective morbidity.

Fear conditioning involves the amygdala as the main neural structure for learning fear responses whereas fear extinction mainly activates the inhibitory prefrontal cortex (PFC). In this study we investigated whether individual differences in trait anxiety affect amygdala and dorsal anterior cingulate cortex (dACC) activation during fear conditioning and extinction.

Thirty-two healthy subjects were investigated by functional magnetic resonance imaging (fMRI) at 3 T while performing a cued fear-conditioning task. All participants completed the trait version of the State-Trait Anxiety Inventory (STAI-T). Activations of the amygdala and the dACC were examined with respect to the effects of trait anxiety.

Analysis of the fMRI data demonstrated enhanced activation in fear-related brain areas, such as the insula and the ACC, during both fear conditioning and extinction. Activation of the amygdala appeared only during the late acquisition phase whereas deactivation was observed during extinction. Regression analyses revealed that highly trait-anxious subjects exhibited sustained amygdala activation and reduced dACC involvement during the extinction of conditioned responses.

This study reveals that high levels of trait anxiety are associated with both increased amygdala activation and reduced dACC recruitment during the extinction of conditioned fear. This hyper-responsitivity of the amygdala and the deficient cognitive control during the extinction of conditioned fear in anxious subjects reflect an increased resistance to extinct fear responses and may thereby enhance the vulnerability to developing anxiety disorders.

Nicotine dependence has been shown to represent a heritable condition, and several research groups have performed linkage analysis to identify genomic regions influencing this disorder though only a limited number of the findings have been replicated.

In the present study, a genome-wide linkage scan for nicotine dependence was conducted in a community sample of 950 probands and 1204 relatives recruited through the University of California, San Francisco (UCSF) Family Alcoholism Study. A modified version of the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) with additional questions that probe nicotine use was used to derive DSM-IV nicotine dependence diagnoses.

A locus on chromosome 2q31.1 at 184 centiMorgans nearest to marker D2S2188 yielded a logarithm (base 10) of odds (LOD) score of 3.54 (point-wise empirical p=0.000012). Additional peaks of interest were identified on chromosomes 2q13, 4p15.33-31, 11q25 and 12p11.23-21. Follow-up analyses were conducted examining the contributions of individual nicotine dependence symptoms to the chromosome 2q31.1 linkage peak as well as examining the relationship of this chromosomal region to alcohol dependence.

The present report suggests that chromosome 2q31.1 confers risk to the development of nicotine dependence and that this region influences a broad range of nicotine dependence symptoms rather than a specific facet of the disorder. Further, the results show that this region is not linked to alcohol dependence in this population, and thus may influence nicotine dependence specifically.

The beneficial outcomes associated with moderate compared with low alcohol intake or abstinence may be due to the inclusion of people as ‘low consumers’, who have stopped consumption because of poor health. We investigated the association between alcohol abstinence and symptoms of common mental disorder and personality disorder, distinguishing between lifelong abstinence and abstinence following previous consumption.

Analyses were based on the British National Survey of Psychiatric Morbidity 2000, which sampled 8580 residents aged 16–74 years. Hazardous drinking (Alcohol Use Disorders Identification Test) was excluded. Symptoms of common mental disorder (depression/anxiety) were identified by the Clinical Interview Schedule. The screening questionnaire of the Structured Clinical Interview for Axis II Personality Disorders was used to identify potential personality disorder. Self-reported alcohol abstinence was divided into lifelong abstinence and previous consumption. Previous consumers were asked why they had stopped. Covariates included socio-economic status, social activity and general health status.

After adjustment, alcohol abstinence was associated with both common mental disorder symptoms and any personality disorder, but only for previous consumers, in whom odds ratios were 1.69 (95% CI 1.23–2.32) and 1.45 (95% CI 1.09–1.94). Associations were non-specific, being apparent for most individual mental disorder symptoms and personality disorder categories. More detailed analysis indicated that associations were again limited to previous consumers who reported ceasing alcohol consumption for health reasons.

Worse mental health in low alcohol consumers, particularly those who have previously ceased for health reasons, should be taken into account when interpreting associations between moderate (compared with low) alcohol consumption and beneficial health outcomes.

Three cognitive constructs are risk factors for eating disorders: undue influence of weight and shape, concern about weight and shape, and body dissatisfaction (BD). Undue influence, a diagnostic criterion for eating disorders, is postulated to be closely associated with self-esteem whereas BD is postulated to be closely associated with body mass index (BMI). We understand less about the relationships with concern about weight and shape. The aim of the current investigation was examine the degree of overlap across these five phenotypes in terms of latent genetic and environmental risk factors in order to draw some conclusions about the similarities and differences across the three cognitive variables.

A sample of female Australian twins (n=1056, including 348 complete pairs), mean age 35 years (s.d.=2.11, range 28–40), completed a semi-structured interview about eating pathology and self-report questionnaires. An independent pathways model was used to investigate the overlap of genetic and environmental risk factors for the five phenotypes.

In terms of variance that was not shared with other phenotypes, self-esteem emerged as being separate, with 100% of its variance unshared with the other phenotypes, followed by undue influence (51%) and then concern (34%), BD (28%) and BMI (32%).

In terms of shared genetic risk, undue influence and concern were more closely related than BD, whereas BMI and BD were found to share common sources of risk. With respect to environmental risk factors, concern, BMI and BD were more closely related to each other than to undue influence.

Anorexia nervosa (AN), at the stage of starvation and emaciation, is characterized by abnormalities in cognitive function, including memory performance. It is unclear whether memory impairment persists or is reversible following weight restoration, and whether memory function differs between AN subtypes. The aim of the present study was to investigate general memory performance in currently ill and fully weight-restored patients of different AN subtypes.

Memory performance was assessed using the Wechsler Memory Scale-Revised (WMS-R) in a total of 99 participants, including 34 restricting-type AN patients (AN-RESTR), 19 binge-eating/purging-type AN patients (AN-PURGE), 16 weight-restored AN patients (AN-W-R) and 30 healthy controls (CONTROL). Cognitive evaluation included a battery of standardized neuropsychological tasks for validating the findings on memory function.

Deficits were found with respect to immediate and delayed story recall in currently ill AN patients irrespective of AN subtype. These deficits persisted in weight-restored AN patients. Currently ill and weight-restored AN patients did not differ significantly from healthy controls with respect to working memory or other measures of neuropsychological functioning.

The findings suggest that impaired memory performance is either a stable trait characteristic or a scar effect of chronic starvation that may play a role in the development and/or persistence of the disorder.

Studies investigating neurocognitive impairment in subjects with eating disorders (EDs) have reported heterogeneous patterns of impairment and, in some instances, no dysfunction. The present study aimed to define the pattern of neurocognitive impairment in a large sample of bulimia nervosa (BN) patients and to demonstrate that neuroendocrine, personality and clinical characteristics influence neurocognitive performance in BN.

Attention/immediate memory, set shifting, perseveration, conditional and implicit learning were evaluated in 83 untreated female patients with BN and 77 healthy controls (HC). Cortisol and 17β-estradiol plasma levels were assessed. Cloninger's Temperament and Character Inventory – Revised (TCI-R), the Bulimic Investigation Test Edinburgh (BITE) and the Montgomery–Asberg Depression Rating Scale (MADRS) were administered.

No impairment of cognitive performance was found in subjects with BN compared with HC. Cortisol and ‘Self-directedness’ were associated with better performance on conditional learning whereas 17β-estradiol had a negative influence on this domain; ‘Reward dependence’ was associated with worse performance on implicit learning; and depressive symptomatology influenced performance on the Wisconsin Card Sorting Test (WCST) negatively.

No cognitive impairment was found in untreated patients with BN. Neuroendocrine, personality and clinical variables do influence neurocognitive functioning and might explain discrepancies in literature findings.

Traumatic life events are generally more common in patients with borderline personality disorder (BPD) than in non-patients or patients with other personality disorders. This study investigates whether exposure to life events moderates the genetic architecture of BPD features. As the presence of genotype–environment correlation (rGE) can lead to spurious findings of genotype–environment interaction (G×E), we also test whether BPD features increase the likelihood of exposure to life events.

The extent to which an individual is at risk to develop BPD was assessed with the Personality Assessment Inventory – Borderline features scale (PAI-BOR). Life events under study were a divorce/break-up, traffic accident, violent assault, sexual assault, robbery and job loss. Data were available for 5083 twins and 1285 non-twin siblings. Gene–environment interaction and correlation were assessed by using structural equation modelling (SEM) and the co-twin control design.

There was evidence for both gene–environment interaction and correlation. Additive genetic influences on BPD features interacted with the exposure to sexual assault, with genetic variance being lower in exposed individuals. In individuals who had experienced a divorce/break-up, violent assault, sexual assault or job loss, environmental variance for BPD features was higher, leading to a lower heritability of BPD features in exposed individuals. Gene–environment correlation was present for some life events. The genes that influence BPD features thus also increased the likelihood of being exposed to certain life events.

To our knowledge, this study is the first to test the joint effect of genetic and environmental influences and the exposure to life events on BPD features in the general population. Our results indicate the importance of both genetic vulnerability and life events.

Twin and sibling studies have identified specific cognitive phenotypes that may mediate the association between genes and the clinical symptoms of attention deficit hyperactivity disorder (ADHD). ADHD is also associated with lower IQ scores. We aimed to investigate whether the familial association between measures of cognitive performance and the clinical diagnosis of ADHD is mediated through shared familial influences with IQ.

Multivariate familial models were run on data from 1265 individuals aged 6–18 years, comprising 920 participants from ADHD sibling pairs and 345 control participants. Cognitive assessments included a four-choice reaction time (RT) task, a go/no-go task, a choice–delay task and an IQ assessment. The analyses focused on the cognitive variables of mean RT (MRT), RT variability (RTV), commission errors (CE), omission errors (OE) and choice impulsivity (CI).

Significant familial association (rF) was confirmed between cognitive performance and both ADHD (rF=0.41–0.71) and IQ (rF=−0.25 to −0.49). The association between ADHD and cognitive performance was largely independent (80–87%) of any contribution from etiological factors shared with IQ. The exception was for CI, where 49% of the overlap could be accounted for by the familial variance underlying IQ.

The aetiological factors underlying lower IQ in ADHD seem to be distinct from those between ADHD and RT/error measures. This suggests that lower IQ does not account for the key cognitive impairments observed in ADHD. The results have implications for molecular genetic studies designed to identify genes involved in ADHD.

The methodology commonly used to estimate disease burden, featuring ratings of severity of individual conditions, has been criticized for ignoring co-morbidity. A methodology that addresses this problem is proposed and illustrated here with data from the World Health Organization World Mental Health Surveys. Although the analysis is based on self-reports about one's own conditions in a community survey, the logic applies equally well to analysis of hypothetical vignettes describing co-morbid condition profiles.

Face-to-face interviews in 13 countries (six developing, nine developed; n=31 067; response rate=69.6%) assessed 10 classes of chronic physical and nine of mental conditions. A visual analog scale (VAS) was used to assess overall perceived health. Multiple regression analysis with interactions for co-morbidity was used to estimate associations of conditions with VAS. Simulation was used to estimate condition-specific effects.

The best-fitting model included condition main effects and interactions of types by numbers of conditions. Neurological conditions, insomnia and major depression were rated most severe. Adjustment for co-morbidity reduced condition-specific estimates with substantial between-condition variation (0.24–0.70 ratios of condition-specific estimates with and without adjustment for co-morbidity). The societal-level burden rankings were quite different from the individual-level rankings, with the highest societal-level rankings associated with conditions having high prevalence rather than high individual-level severity.

Plausible estimates of disorder-specific effects on VAS can be obtained using methods that adjust for co-morbidity. These adjustments substantially influence condition-specific ratings.