Influence of Weight Loss on Cognitive Functions: A Pilot Study of a Multidisciplinary Intervention Program for Obesity Treatment.

There is a relationship between obesity and cognitive functioning. Our aim was to assess weight loss influence on global cognition and executive functioning (EF) in adults with obesity under a multidisciplinary weight loss program. In this six-month longitudinal study, we assessed 81 adults (age < 50 years) with body mass index (BMI) ≥ 30. EF and global cognitive performance were evaluated with the Montreal Cognitive Assessment (MoCA), Neuropsychological Battery of Executive Functions (BANFE-2) and Trail Making Test-Part B (TMT-B). Median age was 40.0 years (IQR: 31.5−47, 61% women), and the median BMI was 41.4 (IQR: 36.7−45.9). At a six-month follow-up, the mean weight loss was 2.67% (29.6% of patients achieved ≥5% weight loss). There was an improvement in EF evaluated with BANFE (p = 0.0024) and global cognition with MoCA (p = 0.0024). Women experienced more remarkable change, especially in EF. Weight loss did not correlate with cognitive performance, except for TMT-B (r-0.258, p = 0.026). In the regression analysis, only years of education predicted the MoCA score. This study showed that patients improved cognitive performance during the follow-up; nevertheless, the magnitude of weight loss did not correlate with cognitive improvement. Future studies are warranted to demonstrate if patients achieving ≥5% weight loss can improve cognition, secondary to weight loss.

Complete sequence of the ANKK1 gene in Mexican-Mestizo individuals with obesity, with or without binge eating disorder.

BACKGROUND: The aim of this study was to investigate if Mexican-Mestizo individuals with obesity, with or without binge eating disorder (BED), exhibited mutations or other type of genetic variants in the sequence of ANKK1. SUBJECTS AND METHODS: Fifty unrelated individuals (21-53 years of age) with obesity, of Mexican-Mestizo ethnic origin were included; 25 of them had BED and 25 presented obesity without BED. The diagnosis of BED was based on criteria proposed in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). Besides, we also analyzed 100 individuals with normal body mass index. DNA from blood leukocytes was amplified by the polymerase chain reaction and all exons of ANKK1 were sequenced. RESULTS: After ANKK1 sequencing we did not find any mutations; however, we observed various polymorphisms. One polymorphism, rs4938013 in exon 2 showed an association with obesity, whilst rs1800497 (also known as Taq1A) in exon 8, showed an association with BED (P = 0.020). Remarkable, for this study, the number of individuals for both polymorphisms for and additive model was sufficient to derive strong statistical power (80%, with a P < 0.05). CONCLUSIONS: To our knowledge, this constitutes the first report where the complete sequences of ANKK1 has been analyzed in individuals with obesity, with or without BED. No mutations were found; however, one polymorphism was associated with obesity, with or without BED, and another one was associated with BED.

Glutamate levels in the associative striatum before and after 4 weeks of antipsychotic treatment in first-episode psychosis: a longitudinal proton magnetic resonance spectroscopy study.

IMPORTANCE: Increased glutamate levels in the right associative striatum have been described in patients during a first episode of psychosis. Whether this increase would persist after effective antipsychotic treatment is unknown. OBJECTIVES: To compare the glutamate levels in antipsychotic-naive patients with first-episode psychosis in the right associative striatum and right cerebellar cortex using proton magnetic resonance spectroscopy before and 4 weeks after antipsychotic treatment and to compare these results with normative data from sex-matched healthy control subjects. DESIGN, SETTING, AND PARTICIPANTS: Before-after trial in an inpatient psychiatric research unit among 24 antipsychotic-naive patients with first-episode psychosis and 18 healthy controls matched for age, sex, handedness, and cigarette smoking. INTERVENTIONS: Participants underwent 2 proton magnetic resonance spectroscopy studies: patients were imaged at baseline and after 4 weeks of antipsychotic treatment, while controls were imaged at baseline and at 4 weeks after the baseline measurement. Patients were treated with oral risperidone (open label) for 4 weeks with dosages that were titrated on the basis of clinical judgment. MAIN OUTCOMES AND MEASURES: Glutamate levels were estimated using LCModel (version 6.2-1T) and were corrected for the cerebrospinal fluid proportion within the voxel. RESULTS: Patients with first-episode psychosis had higher levels of glutamate in the associative striatum and the cerebellum during the antipsychotic-naive condition compared with controls. After clinically effective antipsychotic treatment, glutamate levels significantly decreased in the associative striatum, with no significant change in the cerebellum. No differences in glutamate levels were observed between groups at 4 weeks. CONCLUSIONS AND RELEVANCE: Increased glutamate levels observed at baseline in patients with first-episode psychosis normalized after 4 weeks of clinically effective antipsychotic treatment. These results provide support for the hypothesis that improvement in clinical symptoms might be related to a decrease in glutamate levels.

Striatal glutamate and the conversion to psychosis: a prospective 1H-MRS imaging study.

Increased glutamate levels in the associative-striatum have been described in subjects at ultra-high risk for psychosis (UHR); nevertheless, it is unclear whether this abnormality predicts the conversion to psychosis. Nineteen subjects at UHR and 26 controls were studied using proton magnetic resonance spectroscopy. Subjects at UHR were clinically followed for 2 yr. Seven UHR subjects (37%) transitioned to a psychotic disorder and the remaining 12 did not exhibit psychotic symptoms at the most recent follow-up. The psychosis transition group had higher glutamate levels compared to both non-transition and control groups (p = 0.02 and p < 0.01, respectively; effect size 1.39). These pilot findings suggest that the conversion to psychosis is associated with increased glutamate levels in the associative-striatum.

Validation of the dimensions of psychosis instrument in Mexican patients with schizophrenia spectrum disorders.

The objective was to determine the psychometric properties of the Dimensions of Psychosis Instrument (DIPI) in Mexican patients with schizophrenia spectrum disorders. One-hundred patients were recruited. Convergent and divergent validity were determined with the positive and negative scores of the Positive and Negative Syndrome Scale; a forced five-factor exploratory principal-components analysis with varimax rotation was developed. Total DIPI score shows an adequate convergent validity. The rotated principal component matrix accounted for 82.1% of the variance. Our study gives further support of the adequacy of the DIPI for the assessment of the five most common subjective experiences related to psychosis.

Higher levels of glutamate in the associative-striatum of subjects with prodromal symptoms of schizophrenia and patients with first-episode psychosis.

The glutamatergic and dopaminergic systems are thought to be involved in the pathophysiology of schizophrenia. Their interaction has been widely documented and may have a role in the neurobiological basis of the disease. The aim of this study was to compare, using proton magnetic resonance spectroscopy ((1)H-MRS), glutamate levels in the precommissural dorsal-caudate (a dopamine-rich region) and the cerebellar cortex (negligible for dopamine) in the following: (1) 18 antipsychotic-naïve subjects with prodromal symptoms and considered to be at ultra high-risk for schizophrenia (UHR), (2) 18 antipsychotic-naïve first- episode psychosis patients (FEP), and (3) 40 age- and sex- matched healthy controls. All subjects underwent a (1)H-MRS study using a 3Tesla scanner. Glutamate levels were quantified and corrected for the proportion of cerebrospinal fluid and percentage of gray matter in the voxel. The UHR and FEP groups showed higher levels of glutamate than controls, without differences between UHR and FEP. In the cerebellum, no differences were seen between the three groups. The higher glutamate level in the precommissural dorsal-caudate and not in the cerebellum of UHR and FEP suggests that a high glutamate level (a) precedes the onset of schizophrenia, and (b) is present in a dopamine-rich region previously implicated in the pathophysiology of schizophrenia.