The efficacy of psychopharmacological treatments has been called into question. Psychiatrists are unfamiliar with the effectiveness of common medical drugs.

To put the efficacy of psychiatric drugs into the perspective of that of major medical drugs.

We searched Medline and the Cochrane Library for systematic reviews on the efficacy of drugs compared with placebo for common medical and psychiatric disorders, and systematically presented the effect sizes for primary efficacy outcomes.

We included 94 meta-analyses (48 drugs in 20 medical diseases, 16 drugs in 8 psychiatric disorders). There were some general medical drugs with clearly higher effect sizes than the psychotropic agents, but the psychiatric drugs were not generally less efficacious than other drugs.

Any comparison of different outcomes in different diseases can only serve the purpose of a qualitative perspective. The increment of improvement by drug over placebo must be viewed in the context of the disease's seriousness, suffering induced, natural course, duration, outcomes, adverse events and societal values.

Previous research suggests that various types of childhood maltreatment frequently co-occur and confer risk for multiple psychiatric diagnoses. This non-specific pattern of risk may mean that childhood maltreatment increases vulnerability to numerous specific psychiatric disorders through diverse, specific mechanisms or that childhood maltreatment engenders a generalised liability to dimensions of psychopathology. Although these competing explanations have different implications for intervention, they have never been evaluated empirically.

We used a latent variable approach to estimate the associations of childhood maltreatment with underlying dimensions of internalising and externalising psychopathology and with specific disorders after accounting for the latent dimensions. We also examined gender differences in these associations.

Data were drawn from a nationally representative survey of 34 653 US adults. Lifetime DSM-IV psychiatric disorders were assessed using the AUDADIS-IV. Physical, sexual and emotional abuse and neglect were assessed using validated measures. Analyses controlled for other childhood adversities and sociodemographics.

The effects were fully mediated through the latent liability dimensions, with an impact on underlying liability levels to internalising and externalising psychopathology rather than specific psychiatric disorders. Important gender differences emerged with physical abuse associated only with externalising liability in men, and only with internalising liability in women. Neglect was not significantly associated with latent liability levels.

The association between childhood maltreatment and common psychiatric disorders operates through latent liabilities to experience internalising and externalising psychopathology, indicating that the prevention of maltreatment may have a wide range of benefits in reducing the prevalence of many common mental disorders. Different forms of abuse have gender-specific consequences for the expression of internalising and externalising psychopathology, suggesting gender-specific aetiological pathways between maltreatment and psychopathology.

Recent studies have examined gene×environment (G×E) interactions involving the monoamine oxidase A (MAOA) gene in moderating the associations between exposure to adversity and antisocial behaviour. The present study examined a novel method for assessing interactions between a single gene and multiple risk factors related to environmental and personal adversity.

To test the hypothesis that the presence of the low-activity MAOA genotype was associated with an increased response to a series of risk factors.

Participants were 399 males from the Christchurch Health and Development Study who had complete data on: (a) MAOA promoter region variable number tandem repeat genotype; (b) antisocial behaviour (criminal offending) to age 30 and convictions to age 21; and (c) maternal smoking during pregnancy, IQ, childhood maltreatment and school failure.

Poisson regression models were fitted to three antisocial behaviour outcomes (property/violent offending ages 15–30; and convictions ages 17–21), using measures of exposure to adverse childhood circumstances. The analyses revealed consistent evidence of G x E interactions, such that those with the low-activity MAOA variant who were exposed to adversity in childhood were significantly more likely to report offending in late adolescence and early adulthood.

The present findings add to the evidence suggesting that there is a stable G x E interaction involving MAOA, a range of adverse environmental and personal factors, and antisocial behaviour across the life course. These analyses also demonstrate the utility of using multiple environmental/personal exposures to test G×E interactions.

In general, mothers with depression experience more environmental and family risk factors, and lead riskier lifestyles, than mothers who are not depressed.

To test whether the exposure of a child to risk factors associated with mental health adds to the prediction of child psychopathology beyond exposure to maternal depression.

In 7429 mother–offspring pairs participating in the Avon Longitudinal Study of Parents and Children in the UK, maternal depression was assessed when the children were aged 1.5 years; multiple risk factor exposures were examined between birth and 2 years of age; and DSM-IV-based externalising and internalising diagnoses were evaluated when the children were 7.5 years of age.

Children of clinically depressed mothers were exposed to more risk factors associated with maternal mental health. Maternal depression increased diagnoses of externalising and internalising disorders, but a substantial portion of these associations was explained by increased risk factor exposure (41% for externalising and 37% for internalising disorders). At the same time, these risk exposures significantly increased the odds of both externalising and internalising diagnoses, over and above the influence of maternal depression.

Children of clinically depressed mothers are exposed to both maternal psychopathology and risks that are associated with maternal mental health. These results may explain why treating mothers with depression shows beneficial effects for children, but does not completely neutralise the increased risk of psychopathology and impairment.

Antidepressant prescribing is widespread. Nonetheless, response to antidepressants is variable. If it was possible to predict response to medication and thus tailor treatment accordingly, this would not only improve patient outcomes but may also have economic benefits.

To test the hypothesis that individuals with more severe depression would benefit more from noradrenaline reuptake inhibitors (NARIs) than selective serotonin reuptake inhibitors (SSRIs) compared with individuals with less severe depression.

Individuals recruited from UK primary care who met ICD-10 criteria for a depressive episode and scored 15 or more on the Beck Depression Inventory (BDI) were randomised to either an SSRI (citalopram 20mg daily) or a NARI (reboxetine 4mg twice daily). Randomisation was by means of a remote automated telephone system. The main outcome was depressive symptoms measured by the BDI total score 6 weeks after randomisation. (Trial registration: ISRCTN31345163.)

In total, 601 participants were randomised (citalopram: n = 298, reboxetine: n = 303). Ninety-one per cent were followed up at 6 weeks (citalopram: n = 274, reboxetine: n = 272). There was little evidence to support an interaction between treatment and severity of depression (interaction term: 0.02, 95% CI −0.59 to 0.62, P = 0.96). Adjustment for potential confounders (age, gender, employment status, history of depression, number of life events and social support) did not affect the findings (interaction term: 0.06, 95% CI −0.54 to 0.66, P = 0.85).

Treatment with NARIs does not confer any advantage over SSRI treatment for outcome in those with more severe depressive illness presenting in primary care.

Depression is a known risk factor for mortality after an acute myocardial infarction. Patients with treatment-responsive depression may have a better prognosis than those with treatment-resistant depression.

We sought to determine whether mortality following acute myocardial infarction was associated with treatment-resistant depression.

Follow-up began after myocardial infarction and continued until death or censorship. Depression was counted as present if diagnosed any time during the study period. Treatment for depression was defined as receipt of 12 or more weeks of continuous antidepressant therapy at a therapeutic dose during follow-up. Treatment-resistant depression was defined as use of two or more antidepressants plus augmentation therapy, receipt of electroconvulsive therapy or use of monoamine oxidase inhibitors. Mean duration of follow-up was 39 months.

During follow-up of 4037 patients with major depressive disorder who had had a myocardial infarction, 6.9% of those with insufficiently treated depression, 2.4% of those with treated depression and 5.0% of those with treatment-resistant depression died. A multivariable survival model that adjusted for sociodemographics, anxiety disorders, beta-blocker use, mortality risk factors and health service utilisation indicated that compared with treated patients, insufficiently treated patients were 3.04 (95% CI 2.12–4.35) times more likely and patients with treatment-resistant depression were 1.71 (95% CI 1.05–2.79) times more likely to die.

All-cause mortality following an acute myocardial infarction is greatest in patients with depression who are insufficiently treated and is a risk in patients with treatment-resistant depression. However, the risk of mortality associated with treatment-resistant depression is partly explained by comorbid disorders. Further studies are warranted to determine whether changes in depression independently predict all-cause mortality.

Mental disorders are associated with increased mortality, but population-based surveys with reliable diagnostic procedures controlling for somatic health status are scarce.

To assess excess mortality associated with depressive, anxiety and alcohol use disorders and the principal causes of death.

In a nationally representative sample of Finns aged 30–70 years, psychiatric disorders were diagnosed with the Composite International Diagnostic Interview. After an 8-year follow-up period, vital status and cause of death of each participant was obtained from national registers.

After adjusting for sociodemographic factors, health status and smoking, depressive (hazard ratio (HR) = 1.97) and alcohol use disorders (HR = 1.72) were statistically significantly associated with mortality. Risk of unnatural death was increased among individuals diagnosed with anxiety disorders or alcohol dependence.

Individuals with depressive and alcohol use disorders have an increased mortality risk comparable with many chronic somatic conditions, that is only partly attributable to differences in sociodemographic, somatic health status and hazardous health behaviour.

A limited number of studies have demonstrated changes in cerebral blood flow (CBF) in older individuals with depression, but there are considerable inconsistencies between studies.

To investigate changes in CBF using arterial spin labelling (ASL) magnetic resonance imaging (MRI) in people with late-life depression and in a similarly aged healthy control group.

Sixty-eight participants (30 healthy individuals, 38 with depression) underwent ASL and T1-weighted MRI scanning. For each individual, regional estimates of separate grey and white matter CBF were obtained. Group differences in CBF and their associations with clinical features were examined.

Significant increases were observed in white matter CBF in patients with depression relative to the control group (F1,65 = 9.7, P = 0.003). Grey matter CBF in lateral frontal, medial frontal, cingulate, central and parietal regions did not significantly differ between groups (F1,65≤2.1, P≥0.2). A significant correlation was found between white matter CBF and Montgomery–Åsberg Depression Rating Scale (MADRS) scores in depression (r’ =–0.42, P = 0.03). Further analyses revealed that compared with controls, significant elevation of white matter CBF was apparent in participants whose depression was in remission (n = 21, MADRS≤10, P = 0.001) but not in those with current depression (n = 17, MADRS≥11, P = 0.80).

Findings suggest a compensatory response to white matter pathological change or a response to (or a predictor of) successful antidepressant treatment, perhaps by facilitating neurotransmission in specific circuits and so reducing depressive symptoms.