To conduct a critical review of recent empirical research regarding mood, behaviour and nutrition factors including essential fatty acids, macronutrients, micronutrients and food additives.

A literature search of databases Medline, PsycInfo, CINAHL and Embase up to October 2008. The search emphasised empirical research published in the last 10 years and also included older literature. Studies in both adults and children were addressed.

Research into omega-3 fatty acids has been substantial but evidence for their potential in treating mood and behaviour is modest. In comparison, there has been much less research into carbohydrate and protein intakes and little evidence for their ability to influence mood and behaviour. Recent trials with food additives suggest their removal from the diet may benefit susceptible children with hyperactivity disorders. Micronutrient supplementation appears to improve mood only in those who were initially deficient in micronutrients.

More stringent research designs such as longitudinal studies and the use of biologically inert placebos within randomised controlled trials are needed before supplemental use of omega-3 fatty acids to treat disorders of mood and behaviour can be recommended. Caution is advised regarding the indiscriminate use of diets free of artificial food additives in managing hyperactivity disorders, as they may place an undue burden on individuals and their families. Should omega-3 fatty acid supplementation or the elimination of certain food additives be established as effective, they may provide cost-effective, accessible and well-tolerated adjuncts to standard psychiatric treatments for mood and behavioural disturbances.

There is a lack of clarity about the most useful intervention for functional non-epileptic attacks (FNEA). Outcomes for this condition remain often poor, with considerable personal, social and economic impact. In order to guide clinical practice and future research in this area, we have performed a systematic review of the published literature on the psychological treatment of FNEA.

A comprehensive literature search was carried out using key words: non-epileptic seizures; psychogenic seizures; psychogenic non-epileptic seizures; pseudoseizures; funny turns; non-epileptic attack; hysterical seizures; and pseudoepileptic. Studies specifically looking at psychological treatment of FNEA were identified. Studies of patients also having comorbid organic seizure disorders were excluded.

17 studies that met the inclusion criteria were identified. A broad variety of psychological interventions for FNEA has been investigated. Only one randomised controlled trial has been completed to date. Existing evidence appears to suggest that various psychological treatments, including presenting the diagnosis, psychoeducation, behavioural therapies and mixed modality treatments, may be effective.

While a range of psychological treatments may be beneficial for this patient group, we do not have clear evidence to suggest which treatment is most efficacious. Specific elements of presenting the diagnosis and psychoeducation may be required in addition to traditional cognitive behavioural therapeutic approaches. Large, methodologically robust studies are urgently required to establish the most effective form of treatment.

To provide a selected overview of the literature on psychosocial treatments for bipolar disorder

Selective literature review

Randomised controlled trials of psychosocial interventions in bipolar disorder fall largely into five categories, namely: psychoeducation, integrated treatments, family based therapy, cognitive behavioural therapy and interpersonal social rhythm therapy. Most studies have shown some benefit in terms of relapse prevention, but have tended to be effective for either the depressed or the manic pole, and not both. Broader outcome parameters such as quality of life have not been reported consistently. The mechanisms whereby treatments might exert their effects have not been clearly delineated. Many studies have excluded patients with bipolar II and other variants, and those with psychiatric and substance use comorbidities, reducing their generalisability.

Whilst psychosocial treatments show promise in the area of bipolar disorder, more work is required to delineate the effective elements of such interventions, and to ensure generalisability to individuals with bipolar II and other forms of bipolar disorder, as well as those with psychiatric and substance use comorbidities. Other forms of delivery, such as via the internet, deserve further exploration.

Comparing schizophrenia patients on the basis of familial and non-familial forms of the illness provides a promising approach to the identification of genes involved in schizophrenia. The aim of this study was to search for somatic factors that discriminate between patients with and without a family history of schizophrenia and between their relatives.

Ninety-five schizophrenia patients were structurally interviewed about mental and physical health and alcohol and substance use in themselves and their families. Besides this, complementary information was obtained from the patients’ case records. Patients with (41%) and without (59%) a family history were then compared.

The main differences were found in the patients’ relatives. Fewer patients with a family history, compared with patients without a family history, had relatives with cancer (p = 0.002). Conversely, there was a tendency towards that more patients with a family history, compared with patients without a family history, had relatives with cardiac infarction (p = 0.05).

The genetic risk associated with schizophrenia seems to cosegregate into a factor(s) that protects against cancer and possibly also increases the risk for cardiac infarction.

Genetic factors are largely implicated in predisposing to schizophrenia. Environmental factors contribute to the onset of the disorder in individuals at increased genetic risk. Cognitive deficits have emerged as endophenotypes and potential therapeutic targets for schizophrenia because of their association with functional outcome. The aims of this review were to analyse the joint effect of genetic and environmental (G×E) factors on liability to schizophrenia and to investigate relationships between genes and cognitive endophenotypes focusing on practical applications for prevention and rehabilitation.

Medline search of relevant studies published between 1990 and 2008.

In schizophrenia, examples of G×E interaction include the catechol-O-methyl transferase (COMT) (Val158Met) polymorphism, which was found to moderate the onset of psychotic manifestations in response to stress and to increase the risk for psychosis related to cannabis use, and neurodevelopmental genes such as AKT1 (serine-threonine kinase), brain-derived neurotrophic factor (BDNF), DTNBP1 (dysbindin) and GRM3 (metabotropic glutamate receptor 3), which were associated with development of schizophrenia in adulthood after exposure to perinatal obstetric complications. Neurocognitive deficits are recognised as core features of schizophrenia that facilitate the onset of the disorder and have a great impact on functional outcome. Neurocognitive deficits are also endophenotypes that have been linked to a variety of genes [COMT, neuregulin (NRG1), BDNF, Disrupted-In-Schizophrenia 1 (DISC1) and dysbindin] conferring susceptibility to schizophrenia. Recently, it has emerged that cognitive improvement during rehabilitation therapy was under control of COMT (Val158Met) polymorphism.

This review could indicate a pivotal role of psychiatric genetics in prevention and rehabilitation of schizophrenic psychoses.