People with psychosis are at higher risk of cardiovascular events, partly explained by a higher predisposition to gain weight. This has been observed in studies on individuals with a first-episode psychosis (FEP) at short and long term (mainly up to 1 year) and transversally at longer term in people with chronic schizophrenia. However, there is scarcity of data regarding longer-term (above 3-year follow-up) weight progression in FEP from longitudinal studies. The aim of this study is to evaluate the longer-term (10 years) progression of weight changes and related metabolic disturbances in people with FEP.

Two hundred and nine people with FEP and 57 healthy participants (controls) were evaluated at study entry and prospectively at 10-year follow-up. Anthropometric, clinical, and sociodemographic data were collected.

People with FEP presented a significant and rapid increase in mean body weight during the first year of treatment, followed by less pronounced but sustained weight gain over the study period (Δ15.2 kg; SD 12.3 kg). This early increment in weight predicted longer-term changes, which were significantly greater than in healthy controls (Δ2.9 kg; SD 7.3 kg). Weight gain correlated with alterations in lipid and glycemic variables, leading to clinical repercussion such as increments in the rates of obesity and metabolic disturbances. Sex differences were observed, with women presenting higher increments in body mass index than men.

This study confirms that the first year after initiating antipsychotic treatment is the critical one for weight gain in psychosis. Besides, it provides evidence that weight gain keep progressing even in the longer term (10 years), causing relevant metabolic disturbances.

Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.

To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.

Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.

Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.

AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.

Antipsychotic-induced hyperprolactinemia is associated with relevant side effects: short-term as hypogonadism, gynecomastia, amenorrhoea, sexual dysfunction and galactorrhoea; long-term as cardiovascular disease, bone demineralization and breast and prostate tumors.

To evaluate the effect of switching to long-acting injectable aripiprazole on long-lasting antypsychotic-induced hyperprolactinemia.

This was a prospective observational 1-year study carried out in 125 outpatients with schizophrenia who were clinically stabilized but a switching to another antipsychotic was indicated. We measured the basal prolactine at the start of the study and 1 year after switching to long acting injecatable (LAI) aripiprazole.

In basal analytic, 48% had hyperprolactinemia (21.8–306.2 ng/mL) and 66.5% of them described side effects: 78% sexual dysfunction (72% men), 11% galactorrhoea (100% women), 5.5% amenorrhoea and 5.5% bone pain (100% women). In 48% of patients with hyperprolactinemia, the previous antipsychotics comprised: LAI-paliperidone (65,7%), oral-risperidone (7%), oral-olanzapine (6.1%), oral-paliperidone (5.2%), LAI-risperidone (4%) and others (12%). One year after switching to LAI-aripiprazole, prolactine levels were lower in all patients and in 85% prolactine levels were normalized. Overall, 72% described a clinical improvement, especially in terms of sexual dysfunction.

Several studies have described an improvement of drug-induced hyperprolactinemia after switching to or adding oral aripiprazole. In our study, we observed that levels of prolactine were normalized in 85% of patients with a clinical improvement in almost all of cases. These findings suggest that switching to LAI aripiprazole may be an effective alternative for managing antipsychotic-induced hyperprolactinemia due to its partial agonism in D2 brain receptors, especially in tuberoinfundibular pathway.

The authors have not supplied their declaration of competing interest.

To calculate the 1-year prevalence of schizophrenia and related disorders in a catchment area of Malaga (Spain) and determine the prevalence by gender, dwelling (rural or urban) and socioeconomic area (deprived or non-deprived area).

This cross-sectional study comprised the mental health area covered by Carlos Haya Hospital. We used multiple large clinical databases and key informants to identify cases.

The mean 1-year prevalence of schizophrenia and related disorders was 6.27 per 1000. It was nearly double in men (8.45 per 1000) than in women (4.26 per 1000) (p < 0.001), with a male-to-female ratio of 1.98. The rate was higher in urban (6.64 per 1000) than rural areas (3.95 per 1000) (p < 0.0001) and in socioeconomic deprived areas (7.56 per 1000) than non-deprived areas (6.12 per 1000) (p = 0.005). For the subgroup of schizophrenia, the rates were: men, 5.88 per 1000 and women, 2.2 per 1000 (p < 0.0001), with a male-to-female ratio of 2.67. The rate was also higher in urban (4.2 per 1000) than rural areas (2.49 per 1000) (p < 0.0001) and in socioeconomic deprived areas (4.49 per 1000) than non-deprived areas (3.9 per 1000) (p = 0.149).

The use of multiple clinical sources of information not only from mental health services, but also from emergency departments, primary care and private settings revealed high prevalence rates of schizophrenia and related disorders. This diagnosis is more common in men and in cities. Such precise estimates of the prevalence of schizophrenia have important repercussions for resource allocation and policy planning.

The longitudinal neuropsychological study of first-episode early-onset psychosis (EOP) patients, whose brain maturation is still in progress at the time of illness onset, provides a unique opportunity to compare their cognitive development with that of healthy subjects, in search of specific patterns resulting from the interaction between neurodevelopmental processes and the presence of psychotic disorders.

Seventy-five first-episode EOP patients (schizophrenia n = 35; bipolar disorder n = 17; other forms of psychosis n = 23) with a mean age of 15.53 years were assessed with a neuropsychological battery that included measures of attention, working memory, memory and executive functions within 6 months following the onset of the first psychotic symptom (baseline) and 2 years later. Psychotic symptoms were assessed at both times with the Positive and Negative Symptom Scale (PANSS). Seventy-nine healthy subjects matched for age and education served as controls.

EOP patients showed significant cognitive impairment at both baseline and the 2-year follow-up, with no significant differences between diagnostic groups at either time. Both healthy controls and EOP patients improved in all cognitive measures, except for patient working memory. Improvement in patient attention lost significance after controlling for psychotic symptom reduction. No significant time/diagnosis interaction was found among patients (p > 0.405).

Cognitive impairment in EOP is already present at the first episode, and cognitive development seems to be arrested early in EOP patients compared to their healthy peers, at least for some cognitive functions. These and previous similar results support the neurodevelopmental hypothesis of psychosis.