Low levels of blood cholesterol have been found in some children with autism spectrum disorders (ASD). Psychotropic medications, commonly used by people with ASD and people with intellectual disabilities (ID) are frequently associated with altered metabolic profiles.

We aimed to compare metabolic features of adults with ASD or ID with those of a community-based population.

Data on blood fasting glucose (FBG), lipid profile, liver enzyme profile, TSH, BMI, medications and diagnoses of 80 adults with ASD, 77 adults with ID and 828 control adults were drawn from medical charts/database. Candidates that used glucose or lipid lowering medications were not included.

Total-cholesterol levels of people with ASD and ID were significantly lower than those of the controls (168.3 ± 32.78, 168.2 ± 32.91, 185.4 ± 40.49 mg/dL, respectively, P < 0.001) but after adjusting for gender, age and BMI and using Bonferroni correction, the significance was lost. Compared to controls, ASD and ID had significantly lower FBG (by –14.45 ± 1.81, –14.58 ± 1.54 mg/dl, respectively; P < 0.001 for both) and liver enzymes, despite using psychotropic medications.

In contrast to other psychiatric patients receiving similar medications, people with ASD and ID have unaltered lipid profiles and lower glucose and liver enzyme levels compared to a community-based population.

As weight-gain and metabolic abnormalities during treatment with psychotropic drugs are of great concern, we evaluated effects of psycho-education and medical monitoring on metabolic changes among severely mentally ill patients.

During repeated, systematic psycho-education about general health among 66 consecutive patients diagnosed with DSM-IV-TR schizophrenia (n = 33) or type-I bipolar disorder (n = 33), we evaluated (at intake 1, 2, 3, and 6 months) clinical psychiatric status, treatments and doses, recorded physiological parameters, and assessed attitudes about medication.

At intake, patients with schizophrenia vs bipolar disorder were receiving 3–7 times more psychotropic medication, with 14% higher initial body-mass index (BMI: 29.1 vs 25.6 kg/m2), 12 times more obesity, and significantly higher serum lipid concentrations. During 6-months follow-up, among bipolar disorder patients, polytherapy and serum lipid concentrations declined more than among schizophrenia patients (e.g., total cholesterol + triglycerides, by 3.21 vs 1.75%/month). BMI remained stable. Declining lipid levels were associated with older age, bipolar disorder, being unemployed, higher antipsychotic doses, and lower initial BPRS scores (all P ≤ 0.001).

Psychotropic treatments were more complex, and metabolic measures more abnormal among bipolar disorder than schizophrenia patients. Intensive psycho-education, clinical monitoring, and encouragement of weight-control for six months were associated with improvements in metabolic measures (but not to BMI), and more realistic attitudes about medication.

Serotonin transporter (SERT) and dopamine transporter (DAT) levels differ in patients with major depressive disorder (MDD) who are in a depressed state in comparison with healthy controls. In addition, a family history of depression is a potent risk factor for developing depression, and inherited vulnerability to serotonergic and dopaminergic dysfunction is suspected in this. The aim of this study was to examine the availabilities of midbrain SERT and striatal DAT in healthy subjects with and without a first-degree family history of MDD.

Eight healthy subjects with first-degree relatives with MDD and 16 sex- and age-matched healthy controls were recruited. The availabilities of SERT and DAT were approximated using SPECT, employing [123I] 2-((2-((dimethylamino)methyl)phenyl)thio)-5-iodophenylamine (ADAM) and [99mTc] TRODAT-1 as the ligands, respectively. There are missing data for one participant with a first-degree family history of MDD from the ADAM study, due to a lack of the radio-ligand at the time of experiment.

SERT availability in the midbrain was significantly lower in subjects with a first-degree family history of MDD than in healthy subjects. However, DAT availability was no different between two groups.

The results with regard to the midbrain SERT level suggest the heritability of MDD.

To examine the predictive diagnostic value of affective symptomatology in a first-episode psychosis (FEP) sample with 5 years’ follow-up.

Affective dimensions (depressive, manic, activation, dysphoric) were measured at baseline and 5 years in 112 FEP patients based on a factor structure analysis using the Young Mania Rating Scale and Hamilton Depression Rating Scale. Patients were classified as having a diagnosis of bipolar disorder at baseline (BDi), bipolar disorder at 5 years (BDf), or “other psychosis”. The ability of affective dimensions to discriminate between these diagnostic groups and to predict a bipolar disorder diagnosis was analysed.

Manic dimension score was higher in BDi vs. BDf, and both groups had higher manic and activation scores vs. “other psychosis”. Activation dimension predicted a bipolar diagnosis at 5 years (odds ratio = 1.383; 95% confidence interval, 1.205–1.587; P = 0.000), and showed high levels of sensitivity (86.2%), specificity (71.7%), positive (57.8%) and negative predictive value (90.5%). Absence of the manic dimension and presence of the depressive dimension were both significant predictors of an early misdiagnosis.

The activation dimension is a diagnostic predictor for bipolar disorder in FEP. The manic dimension contributes to a bipolar diagnosis and its absence can lead to early misdiagnosis.

Except in broad outline, little is known about the most likely symptomatic trajectories in prodromal schizophrenia. The aim of this study is to delineate these pathways.

Taking into account existing clinical knowledge, the causal relationships between the 12 prodrome scales of the Schizotypic Syndrome Questionnaire (SSQ) were examined in a general-population sample by applying the mathematical theory of directed graphs. Use was made of two discovery algorithms implemented in the Tetrad-4 program, as well as of the graphical DAGitty program to test whether a particular model holds.

A promising model was selected that may describe the causal pathways in schizophrenic prodromal unfolding. Testing this model by means of DAGitty, it was shown that the minimal testable implications, listed as conditional independences, and the direct and total effects in the model, identified after correction for bias, were as hypothesized. For practical reasons, a simpler version of the resulting SSQ model, containing only its principal pathways, was provided.

Although resembling an earlier model that was based on a series of LISREL analyses, the present model was believed to provide a more dependable description of schizophrenic prodromal unfolding, as it relies on methods that are less subject to the limitations involved in SEM.

Negative symptoms are known to undermine functional outcomes in people with schizophrenia; however, most studies have not accounted for whether these symptoms were primary or secondary to other psychopathological factors. The present study examined the impact of primary negative symptoms on functional outcomes in patients with schizophrenia.

The sample included 1427 patients with schizophrenia who completed the baseline visit in the CATIE study. Symptoms were assessed with the Positive and Negative Syndrome Scale and Calgary Depression Scale, extrapyramidal side effects with the Simpson-Angus scale, and functional status with the Heinrichs-Carpenter Quality of Life Scale.

Negative symptoms were significantly and inversely related to each domain of functioning examined. These relationships remained after statistically controlling for the influence of potential sources of secondary negative symptoms. In addition, the relationships between negative symptoms and specific domains of functioning remained in patients who had mild/absent positive, depressive, anxiety and extrapyramidal symptoms. Negative symptoms were associated with functional outcomes even in antipsychotic-free patients.

Primary negative symptoms significantly contribute to the functional impairment seen in people with schizophrenia. A better understanding of the etiology and pathobiology of these symptoms is required to guide the search for effective therapeutics that promote functional recovery.

To analyse associations between brain morphology and longitudinal and cross-sectional measures of outcomes in schizophrenia in a general population sample.

The sample was the Northern Finland 1966 Birth Cohort. In 1999–2001, structural brain MRI and measures of clinical and functional outcomes were analysed for 54 individuals with schizophrenia around the age of 34. Sex, total grey matter, duration of illness and the use of antipsychotic medication were used as covariates.

After controlling for multiple covariates, increased density of the left limbic area was associated with less hospitalisations and increased total white matter volume with being in remission. Higher density of left frontal grey matter was associated with not being on a disability pension and higher density of the left frontal lobe and left limbic area were related to better functioning. Higher density of the left limbic area was associated with better longitudinal course of illness.

This study, based on unselected general population data, long follow-up and an extensive database, confirms findings of previous studies, that morphological abnormalities in several brain structures are associated with outcome. The difference in brain morphology in patients with good and poor outcomes may reflect separable aetiologies and developmental trajectories in schizophrenia.