Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic discoveries in eating disorders in the genome-wide era. To date, five genome-wide association studies on eating disorders have been conducted – all on anorexia nervosa (AN). For AN, several risk loci have been detected, and ~11–17% of the heritability has been accounted for by common genetic variants. There is extensive genetic overlap between AN and psychological traits, especially obsessive-compulsive disorder, and intriguingly, with metabolic phenotypes even after adjusting for body mass index (BMI) risk variants. Furthermore, genetic risk variants predisposing to lower BMI may be causal risk factors for AN. Causal genes and biological pathways of eating disorders have yet to be elucidated and will require greater sample sizes and statistical power, and functional follow-up studies. Several studies are underway to recruit individuals with bulimia nervosa and binge-eating disorder to enable further genome-wide studies. Data collections and research labs focused on the genetics of eating disorders have joined together in a global effort with the Psychiatric Genomics Consortium. Molecular genetics research in the genome-wide era is improving knowledge about the biology behind the established heritability of eating disorders. This has the potential to offer new hope for understanding eating disorder etiology and for overcoming the therapeutic challenges that confront the eating disorder field.

This report is concerned with a simple statistical model of the way the brain may function, suggested by the analysis of intelligence test results in two groups of children. The model describes the statistical behaviour of an ideal array of elements, representing the brain, during tests of cognitive ability. Predictions from the model indicate that comparison of the EEC recording taken from groups of children who were good or poor readers would show amplitude differences. These were found between the groups when the eyes were open but not when the eyes were closed–a result explained by the model.

Regional cerebral blood flow (rCBF) was investigated in a group of medicated DSM-III-R schizophrenic patients and age, sex and handedness matched normal volunteers using a split-dose 99mTc-HMPAO Single Photon Emission Tomography (SPET) protocol. Measures were taken during the performance of a verbal memory task aimed at activating the left medial temporal lobe, a region repeatedly suggested to be structurally abnormal in schizophrenia. In normal subjects, the performance of the task was associated with significant rCBF increases in the left medial temporal, left inferior frontal and anterior cingulate cortices, and right cerebellum. Despite their significantly poorer performance on the memory task, the degree of medial temporal activation measured in the schizophrenic patients was not significantly different from that found in the control group. This finding suggests that memory deficits in schizophrenia do not necessarily imply failure to activate the left medial temporal lobe as assessed by 99mTc-HMPAO SPET.

Major depression is reportedly characterized by increased activity of the hypothalamic–pituitary–adrenal (HPA) axis and by in vivo immune activation. The present study was carried out in order to investigate the relationships between HPA-axis activity and in vivo immune function in depression. Towards this end the following parameters were measured: 24 h urinary cortisol (UC) excretion; basal and post-dexamethasone (DST) plasma cortisol, β-endorphin/β-lipotropin (βEND/βLPH) and dexamethasone concentrations; and leucocyte subsets (i.e. lymphocytes, neutrophils, monocytes, CD4+, CD4+CD45RA+, CD4+CD45RO+, CD8+, CD8+CD57+, CD8+CD57−, HLA-DR+, CD25+ T cells, HLA-DR+, CD19+, CD20+, and CD21+ B cells) both pre-and post-DST. Dexamethasone administration (1 mg orally) induced leucocytosis, lymphocytopaenia, monocytopaenia and neutrophilia. HPA-axis non-suppressors exhibited a relative resistance to the enhancing (e.g. neutrophils) or depressant (e.g. lymphocytes, CD4+ T cells) effects of dexamethasone. There were significant correlations between UC excretion and the number of percentage of lymphocytes, monocytes, CD4+CD45RA+ and CD8+CD57− T cells (negatively) and neutrophils (positively). It is concluded that multiple and complex intertwined relationships between HPA-axis hyperactivity and systemic immune stimulation participate in the pathophysiology or pathogenesis of major depression.

This preliminary communication reports that the mothers of 104 schizophrenic patients had: (1) a significantly higher incidence of thyroid disease than a carefully matched control group; (2) significantly more abortions, still-births and greater infant mortality. The findings and possible relevance of thyroid disease to schizophrenia are discussed. Three prospective studies currently in progress are outlined.

Sixty-four children taken to court for failure to attend school were reliably classified into 4 groups, according to whether they exhibited the features of ‘school refusal’ and/or ‘truancy’. About a fifth of them were found to exhibit ‘school refusal’; a third showed ‘truancy’; less than a sixth exhibited both ‘school refusal’ and ‘truancy’ combined; and over a third had the characteristics of neither condition. Differences between these categories were found in manifestations of psychiatric disturbance and in responsiveness to a court adjournment procedure.

Foolish as the theory of Durkeim may be in confusing what is religious with what is social, it yet contains an element of truth; that is to say that the social feeling is so much like the religious as to be mistaken for it. (Simone Weil, 1951).

Psychiatrists concern themselves with human mental suffering. Behind the consulting room door they reflect with their patients on questions of meaning and existence, issues that concern philosophy and religion as much as psychiatry. It is striking, therefore, that psychiatrists regard spirituality and religion as, at best, cultural noise to be respected but not addressed directly, or at worst pathological thinking that requires modification (Larson et al. 1993).

Despite two millennia of debate we are little nearer a consensus on the meanings of spirituality and religion. The word ‘religion’ has as many definitions as writers. Spirituality and religion are often used interchangeably. Spilka (1985) doubts that a single definition is even possible. Dittes (1969) argues that religion contains so many unrelated variables that it cannot be considered as a unidimensional concept in research. We would argue that religion is the outward practice of a spiritual system of beliefs, values, codes of conduct and rituals (Speck, 1988). Religious groups may function like any other with codes of behaviour, political alliances and ‘in’ and ‘out’ group member ideology (Sherif et al. 1966).

Unfortunately, a concentration on the religious variable has led to a failure to appreciate the broader concept of spiritual and the presumption that if someone does not profess a recognized, religious faith, they have no spiritual discernment or need (Speck, 1988). We propose a definition of ‘spiritual’ as a person's experience of, or a belief in, a power apart from their own existence. It may exist within them but is ultimately apart. It is the sense of relationship or connection with a power or force. It is more specific than a search for meaning or a feeling of unity with others. People may use the word ‘spiritual’ to describe intense emotional pleasure when moved by natural beauty or by an important relationship. Spiritual belief is more specific than that. Some people may use the word ‘God’ to describe this power; others may be less specific. Spirituality differs from belief in other powers, such as nuclear power or magnetism, in its ‘set apart’ quality and the degree to which it is revered and ritualized, the quality which Durkheim (1915) refers to as the sacred.

Background. In schizophrenia, affective disorders, and obsessive–compulsive disorder (OCD) dysfunction of frontal neuronal circuits has been suggested. Such impairments imply corresponding oculomotor deficits.

Method. Eye movement response to foveofugal and foveopetal step–ramp stimuli was recorded within the same study design in patients with schizophrenia (N=16), affective disorder (N=15), and OCD (N=18) and compared with controls (N=23) using infra-red reflection oculography.

Results. In the foveofugal task steady-state velocity was lower in all patient groups compared with controls. Post-saccadic eye velocity was also decreased in patients with schizophrenia and affective disorder. In the foveopetal stimulus steady-state velocity was reduced in schizophrenic patients, only. Changes of saccadic latencies or position errors were not found in any of the patient groups. Also, pursuit latency was unchanged and initial eye acceleration was not decreased.

Conclusions. Unaltered saccadic parameters indicate intact motion perception in cortical visual area V5. Therefore, the observed deficit of pursuit maintenance implies a dysfunction of frontal networks in all patient groups including the pursuit region of the frontal eye field (FEF). In patients with schizophrenia and affective disorder reduced post-saccadic pursuit initiation may indicate an impaired interaction between the pursuit and the saccadic system.

Background. Carers of patients with clinical dementia have increased rates of depressive illness but the biological mechanisms by which the stress of caring can lead to mood disorders is not well understood.

Methods. We recruited 30 full-time carers of patients with dementia and 28 age and gender-matched controls. None of the subjects were suffering from a significant depressive disorder. We measured salivary cortisol at four time points throughout a single day and also took a single fasting morning blood sample for plasma tryptophan.

Results. Salivary cortisol levels were significantly higher in carers than controls at 12.00 h and 22.00 h. Plasma total tryptophan but not free tryptophan levels were significantly lower in carers.

Conclusions. The changes found in these non-depressed carers were essentially similar to those in patients with major depression. We suggest that increased cortisol secretion and lowered tryptophan availability increase the risk of mood disorders in carers.

A clinical trial was undertaken to assess the effectiveness of social work intervention with a group of depressed women attending their general practitioner for treatment. Social work treatment was ineffective for the group of women as a whole on changes in social scores, clinical ratings, or visits to the doctor. The results suggest, however, that social work help benefited those with ‘acute on chronic’ illness but had no effect on those with more acute conditions.

A significant proportion of the global burden of disease can be attributed to mental illness. Despite important advances in identifying risk factors for mental health conditions, the biological processing underlying causal pathways to disease onset remain poorly understood. This represents a limitation to implement effective prevention and the development of novel pharmacological treatments. Epigenetic mechanisms have emerged as mediators of environmental and genetic risk factors which might play a role in disease onset, including childhood adversity (CA) and cannabis use (CU). Particularly, human research exploring DNA methylation has provided new and promising insights into the role of biological pathways implicated in the aetio-pathogenesis of psychiatric conditions, including: monoaminergic (Serotonin and Dopamine), GABAergic, glutamatergic, neurogenesis, inflammatory and immune response and oxidative stress. While these epigenetic changes have been often studied as disease-specific, similarly to the investigation of environmental risk factors, they are often transdiagnostic. Therefore, we aim to review the existing literature on DNA methylation from human studies of psychiatric diseases (i) to identify epigenetic modifications mapping onto biological pathways either transdiagnostically or specifically related to psychiatric diseases such as Eating Disorders, Post-traumatic Stress Disorder, Bipolar and Psychotic Disorder, Depression, Autism Spectrum Disorder and Anxiety Disorder, and (ii) to investigate a convergence between some of these epigenetic modifications and the exposure to known risk factors for psychiatric disorders such as CA and CU, as well as to other epigenetic confounders in psychiatry research.

Background. Numerous studies have documented high rates of co-morbidity between major depressive disorder (MDD) and the anxiety disorders (ANX). However, the reason for this is unclear. Family studies provide one potentially useful approach for addressing this issue.

Method. We explored six explanations of the co-morbidity between MDD and ANX using a family study of a large community sample of young adults and their first-degree relatives. Participants included 112 probands with a lifetime history of both MDD and one or more ANX, 290 probands with a history of MDD but no ANX, 43 probands with a history of one or more ANX but no MDD, 352 probands with no lifetime history of either MDD or ANX, and the probands' 2608 first-degree relatives. Probands were assessed using semi-structured diagnostic interviews on two occasions in adolescence and a third time at age 24. Diagnostic data on relatives were collected using both direct and family history interviews.

Results. Compared with controls, MDD aggregated in the families of probands with MDD, whether or not they had co-morbid ANX; ANX aggregated in the families of probands with ANX, regardless of whether they had co-morbid MDD; and co-morbid MDD/ANX aggregated only in the families of probands with both MDD and ANX. The relatives of probands with ANX alone had a significantly higher rate of ANX than the relatives of probands with MDD alone, although none of the other comparisons between the depressed and anxious groups were significant.

Conclusions. This pattern of findings is largely, although not completely, consistent with the view that MDD and ANX are transmitted independently within families, and suggests that the co-morbidity between MDD and ANX is caused by non-familial aetiological factors.

Leading articles or textbooks on anorexia nervosa generally give credit for its discovery to either the British physician William Withey Gull or to the French neuropsychiatrist Ernest Charles Lasègue. Although the major contributions of both men show a remarkable but independent coincidence around 1873, Gull is mostly given a slight priority because of a rather cryptic mention of an anorexia-like condition in a paper read in 1868. An analysis of the events, however, shows that the British physician from London does not really deserve this honour. For no clear-cut priority for either man can be established.