Tourette syndrome (TS) is a genetically complex disorder for which no causative genes have been unequivocally identified. Nevertheless, a number of molecular genetic studies have investigated several candidate genes, particularly those implicated in dopamine modulation. The results of these studies were inconclusive, which may be due, at least in part, to the variable ethnicity of the patients included in different studies and the chosen research design. In this study, we used a family-based association approach to investigate the implication of dopamine-related candidate genes, which had been previously reported as possibly associated with TS [genes that encode for the dopamine receptors DRD2, DRD3 and DRD4, the dopamine transporter 1 (SLC6A3) and the monoamine oxidase-A (MAO-A). The studied group was composed of 110 TS patients. These patients were selected from the French Canadian population, which displays a founder effect. Excess transmission of the 7-repeat allele of the DRD4 exon-3 VNTR polymorphism (v 2 TDT ¼4.93, 1 df, P¼0.026) and the putative 'high-activity' alleles of the MAO-A promoter VNTR polymorphism (v 2 TDT ¼7.124, 1 df P¼0.0076) were observed. These results were confirmed in a subgroup of patients with no attention deficit/hyperactivity or obsessive compulsive comorbid disorders. Haplotype analysis using one or two supplemental polymorphism in each of these genes confirmed these associations and allowed one to identify risk haplotypes. No associations were found for DRD2, DRD3 or SLC6A3. These data support the notion that DRD4 and MOA-A genes may confer an increased risk for developing TS in the French Canadian population.

In Mexico, gender differences in FGIDs exist, with both IBS and dyspepsia being more common in women than men. In IBS, symptoms related to constipation and bloating were more common in women, but the dyspepsia group was too small to draw any conclusions. Finally, this is the first study to report that belching is more common in men than women controls not fulfilling criteria for any FGID.

Tourette syndrome (TS) is a complex neuropychiatric disorder with a strong genetic basis. Although no specific susceptibility genes have been identified for TS, cytogenetic studies in selected cases suggest the existence of a predisposing gene located in the 7q31 chromosomal region. In order to test the hypothesis of a possible relationship between this region and TS at the population level, we undertook a family based association study in a sample of French Canadian patients from Quebec. For this purpose, markers D7S522, D7S523, and D7S1516 were tested using the extended transmission disequilibrium test (e-TDT). Marker D7S522 showed a biased transmission of alleles from heterozygote parents to their TS offsprings (allele-wise TDT chi(2) = 12.61, 4 df, P = 0.013, genotype-wise TDT chi(2) = 15.49, 7 df, P = 0.030). When the analysis was restricted to patients without ADHD or OCD comorbidity, similar results were observed both allele and genotype-wise (chi(2) = 10.68, 4 df, P = 0.03 and chi(2) = 12.55, 5 df, P = 0.028, respectively). In addition, marker D7S523 was also associated (allele-wise TDT chi(2) = 18.37, 7 df, P = 0.01 and genotype-wise TDT chi(2) = 46.26, 17 df, P = 0.00016), and showed a tendency for association in the comorbidity-free subgroup (genotype-wise TDT chi(2) = 18.7, 10 df, P = 0.044). Finally, marker D7S1516, contained in the inner mitochondrial membrane peptidase 2 like (IMMP2L) gene, also showed a tendency for association (genotype-wise TDT chi(2) = 32.87, 21 df, P = 0.048). These results may reflect the proximity of markers D7S522, D7S523, and possibly D7S1516 to a gene or regulatory region relevant to TS predisposition.

In patients with BD, differences in BMI may be affected by the presence of FTO risk alleles, especially in homozygous individuals for these variants. Besides evaluating the possible metabolic effects of certain antipsychotics or mood stabilizers, it is important to evaluate the role of other factors such as FTO risk alleles.

Aim: The aim of this study was to determine if the problem-solving therapy (PST) helps control metabolic variables in patients with type 2 diabetes mellitus (T2DM) who show depressive and anxiety symptoms. Background: T2DM is a chronic-degenerative multifactorial disease. It is considered one of the main public health problems in the world, and it represents an important social and economic burden. It is frequently associated with major depression and anxiety disorders, which are related with high glycated hemoglobin (HbA 1c ) concentrations and poor metabolic control. Method: We initially included 123 patients diagnosed with T2DM from five primary care centers (PCC) in Mexico City. HbA 1c , central glucose, and lipid profile were measured in each patient. In addition, the Kessler psychological distress scale (K-10), the Beck Depression Inventory, and the Beck Anxiety Inventory were applied at the beginning and, to those who continued, at the end of the PST, as well as four months later. Findings: In total, 36 patients completed the PST and the follow-up. There was a significant decrease in depressive and anxiety symptoms (P < 0.001), as well as in total cholesterol (P = 0.002), HbA 1c (P = 0.05), and low-density lipoprotein (LDL) (P = 0.022). The PST helps reduce depressive and anxiety symptoms and may help stabilize glucose and cholesterol up to four months. Further studies on this area are recommended. If our findings are confirmed, the PST could help improve the quality of life of thousands of individuals with psychiatric-metabolic co-morbidity who only visit PCC.

Introduction Several studies indicate that polygenic obesity is linked to fat‐mass and obesity‐associated ( FTO ) genetic variants. Nevertheless, the link between variants in FTO and mental disorders has been barely explored. The present work aims to determine whether FTO genetic variants are associated with bipolar disorder and obesity, and to perform an in silico prediction of variant‐dependent functional impact on the developing brain transcriptome. Methods Four hundred and forty‐six Mexican mestizos were included in a genetic association analysis. SNP ‐sequence kernel association test and linear mixed models were implemented for genetic association assessment. For functional impact prediction, we analyzed the mapping of regulatory elements, the modification of binding sites of transcription factors and the expression of transcription factors in the brain developing transcriptome, searching on different databases. Results In the set‐based analysis, we found different associated regions to BD (bipolar disorder) and obesity. The promoter flanking region of FTO intron 1 was associated with differential effects on BMI , while intron 2 of RPGRIP 1L and FTO upstream regions were associated with BD . The prediction analysis showed that FTO BD ‐associated variants disturb binding sites of SP 1 and SP 2; obesity‐associated variants, on the other hand, disturb binding sites of FOXP 1, which are transcription factors highly expressed during prenatal development stages of the brain. Conclusion Our results suggest a possible effect of FTO variants on neurodevelopment in obesity and bipolar disorder, which gives new insights into the molecular mechanism underlying this association.

Previous studies have found association and linkage between Tourette syndrome (TS) and markers at the 11q24 region, mainly with markers D11S1377 and D11S933. In order to determine if these positive findings could be replicated in our sample, we undertook a family-based association study in 199 French Canadian TS nuclear families. We genotyped 572 individuals from 174 complete and 25 incomplete TS trios. TDT analysis failed to detect an association between TS and six markers from 11q24. Furthermore, no haplotype combining alleles from D11S1377, D11S933, or any of the other four markers was associated with the disorder. Linkage disequilibrium analysis showed evidence of historical recombination between every contiguous pair of markers, indicating that these genetic variants are probably in equilibrium in the French Canadian population. Further analysis in additional families, with different methodologies (linkage and association) will be required in order to determine if the 11q24 region harbors a susceptibility locus for TS. If it does, this defect may not be frequent in the French Canadian population due to locus heterogeneity.

A cross-sectional design was used. The study was conducted in two consecutive studies in six PCC that serve marginalized population in Mexico City. In the first study, cases were interviewed, diagnosed, and treated by a psychiatrist. In the second study, Collaborative Care model was used and GPs were trained; psychiatrists diagnosed and treated patients but GPs discussed the symptoms and treatment of the patients with the psychiatrist. Findings First study: 18 patients with depressive and/or anxiety disorders were interviewed; these cases were not discussed between the GPs and the psychiatrist. Second study: psychiatrists and GPs conducted joint interviews and cases were discussed. From the 399 evaluated individuals, 38.94% were diagnosed with a depressive disorder. After the Collaborative Care model was applied, GPs were more aware about mental health problems and they were more interested in the identification of these conditions in PCC. Replication studies will help confirm the effectiveness of this model.