Animal experimental studies suggest that the amino acid valine may decrease brain serotonin (5-HT) function by inhibiting the transport of the 5-HT precursor, L-tryptophan, across the blood barrier. The aim of the present study was to assess whether valine could decrease brain 5-HT function in healthy subjects and provoke symptomatic relapse in recently remitted depressed patients taking antidepressant drug treatment.

We studied the effect of valine (30 g) on the prolactin (PRL) response to the 5-HT releasing agent, d-fenfluramine, in healthy male subjects and on the mood of 12 remitted depressed patients taking either selective serotonin re-uptake inhibitors (n = 10) or lithium and amitriptyline (n = 2).

Valine significantly lowered the PRL response to d-fenfluramine in healthy subjects. In the remitted depressives, valine caused a mild but detectable lowering of mood on a number of measures but only one patient experienced a significant relapse in mood.

Valine administration may decrease brain 5-HT neurotransmission in humans. This effect could explain the mild increase in depressive symptoms in patients taking 5-HT-potentiating drugs.

Little is known about the long-term mortality and causes of death after first psychiatric admission.

A consecutive series of 87 patients admitted for the first time from a strictly defined catchment area to Saxondale Hospital, Nottinghamshire, who were discharged in 1974 and 1975, were traced in 1992 to either their general practitioner or death. The causes of their deaths were ascertained and the observed mortality was compared with expected mortality.

Twelve subjects had died. None had committed suicide, and there were no open verdicts or accidental deaths. Although the observed mortality was higher than expected, there was no significant excess.

There may be little scope for reducing suicide rates by targeting patients for careful follow-up after discharge from their first psychiatric admission. More research is required before large investments are made in potentially fruitless interventions to achieve the objectives of The Health of the Nation.

In 1962 approximately 1.5 million French people living in Algeria were repatriated to France in very poor and often life-threatening conditions. These people constitute a cohort for the study of the long-term impact of gene–environment interaction on depression.

To examine the interaction between a highly stressful life event and subsequent depression, and its modulation by a length polymorphism of the serotonin transporter gene (5–HTTLPR).

A community sample of people aged 65 years and over residing in the Montpellier region of the south of France was randomly recruited from electoral rolls. Genotyping was performed on 248 repatriated persons and 632 controls. Current and lifetime major and minor depressive disorders were assessed according to DSM-IV criteria.

A significant relationship was observed between exposure to repatriation and subsequent depression (P<0.002), but there was no significant effect of gene alone (P = 0.62). After controlling for age, gender, education, disability, recent life events and cognitive function, the gene–environment interaction (repatriation×5-HTTLPR) was globally significant (P<0.002; OR = 3.21, 95% CI 2.48–5.12). Individuals carrying the two short (s) alleles of 5-HTTLPR were observed to be at higher risk (P<0.005; OR = 2.34, 95% CI 1.24–4.32), particularly when repatriation occurred before age 35 years (P<0.002; OR = 2.91, 95% CI 1.44–5.88), but this did not reach significance in those who were older at the time of the event (P = 0.067).

The association between depression and war repatriation was significantly modulated by 5-HTTLPR genotype but this appeared to occur only in people who were younger at the time of exposure.

Sampling techniques for national surveys have constrained the statistical power in estimating prevalence rates of child mental health problems in minority ethnic groups.

To establish the prevalence rates of mental health problems in ethnic Indian adolescents in England and compare these with matched White adolescents living in the same areas.

A cross-sectional survey with oversampling of Indian adolescents aged 13–15 years of age.

The sample size was 2900 (71% response rate) with 1087 (37%) Indian and 414 (14%) White adolescents. Ethnically Indian adolescents had lower rates of all types of mental

health problems (5% v. 13% and 21% v. 30% for abnormal Strengths and Difficulties Questionnaire and Short Mood and Feelings Questionnaire scores, respectively) and substance misuse (18% v. 57%, 5% v. 15% and 6% v. 9% for regular alcohol, smoking and drug use, respectively), with the exception of eating disorders, compared with their White counterparts. The odds of an abnormal score on the mental health questionnaires were worse for White compared with Indian children irrespective of sociodemographic variables.

Factors relating to how Indian adolescents are parented or their social support networks may be influencing their mental health and may warrant further investigation.

Many psychiatrists in the UK may be surprised to find that the Government ratified a convention ten years ago that suggests compulsory mental health treatment be prohibited. The Convention on the Rights of Persons with Disabilities is arguably the most important legal instrument that no one in psychiatry ever discusses, but if moved from ratification to enforcement it would have enormous effect on day-to-day practice. Here, Dr Paul Gosney argues that the convention if enforced would be damaging for the people it aims to protect, whereas Professor Peter Bartlett defends it as a necessary challenge to the inequalities in our current system.

Residential mobility during upbringing, and especially adolescence, is associated with multiple negative mental health outcomes. However, whether associations are confounded by unmeasured familial factors, including genetic liability, is unclear.

We used a population-based case–cohort study to assess whether polygenic risk scores (PRSs) for schizophrenia, bipolar disorder and major depression were associated with mobility from ages 10–14 years, and whether PRS and parental history of mental disorder together explained associations between mobility and each disorder.

Information on cases (n = 4207 schizophrenia, n = 1402 bipolar disorder, n = 18 215 major depression) and a random population sample (n = 17 582), born 1981–1997, was linked between Danish civil and psychiatric registries. Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of separate, large meta-analyses.

PRSs for schizophrenia and major depression were weakly associated with moving once (odds ratio 1.07, 95% CI 1.00–1.16; and odds ratio 1.10, 95% CI 1.04–1.17, respectively), but not twice or three or more times. Mobility was positively associated with each disorder, with more moves associated with greater risk. Adjustment for PRS produced slight reductions in the magnitude of associations. Adjustment for PRS and parental history of mental disorder together reduced estimates by 5–11%. In fully adjusted models mobility was associated with all three disorders; hazard ratios ranged from 1.33 (95% CI 1.08–1.62; one move and bipolar disorder) to 3.05 (95% CI 1.92–4.86; three or more moves and bipolar disorder).

Associations of mobility with schizophrenia, bipolar disorder and depression do not appear to be attributable to genetic liability as measured here. Potential familial confounding of mobility associations may be predominantly environmental in nature.