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Clinical evidence suggests that inflammation is a key factor to understand the causes of depressive symptoms. Fluoxetine is one of the main first-line medications used for depression, and it is hypothesized that it participates in the decrease of pro-inflammatory cytokines. Hence, our aim was to perform a meta-analysis and systematic review to understand the interaction of fluoxetine in the IL-1β, IL-6 and TNF-α inflammatory process. Studies identified in PubMed and Scopus databases were used to perform a meta-analysis via the Comprehensive software. Standardized mean difference (SMD) was used as a summary statistic. The analysis included a total of 292 individuals with major depressive disorder who received fluoxetine for a period longer than 6 weeks; additionally, IL-1β, IL-6 or TNF-α levels were measured at the end of the antidepressant treatment. The findings were significant revealed decreased levels of the cytokines studied. In conclusion, the pooled data suggest that fluoxetine treatment improved depressive symptomatology by the modulation of pro-inflammatory process such as IL-1β, IL-6 or TNF-α.

Psychiatric disorders are complex polygenic diseases that show common genetic vulnerability. Several studies have investigated the association of polymorphisms of FK506 binding protein 51 (FKBP5) gene and depressive disorders or suicidal behavior, however, the results have been controversial and ambiguous. The aim of our study was to explore the role of the FKBP5 gene variants (rs1360780, rs3800373 and rs4713916), in depressive disorders or suicidal behavior through a systematic review and a meta-analysis. The protocol number of the study is PROSPERO CRD42018089295. The meta-analysis included 12 studies. Odds ratios with 95% confidence intervals were used to evaluate the association and the publication bias was tested by Egger's test and funnel plot; heterogeneity was assessed by the Cochran's chi-square-based Q statistic test and the inconsistency index. Our results showed that the rs3800373 and rs4713916 were associated with an increased risk of depressive disorders when using the heterozygous and dominant models. In the stratified analysis by ethnicity, a significantly increased risk of depressive disorders was also observed for rs3800373 and rs4713916 in Caucasians. When we analyzed suicidal behavior, we found a significant association with the rs1360780 of FKBP5 and suicidal behavior risk in the overall population and rs3800373 in completed suicide subgroup. Existing evidence indicates that the polymorphisms of FKBP5 gene are associated with risk of depressive disorders and suicidal behavior. Future studies with larger sample sizes will be necessary to confirm the present results.

Eating disorders (ED) are characterized by disruption of eating behaviour and alteration of food intake. Leptin, is one of the main hormones that modulate food intake and are altered in individuals diagnosed with ED. Genetic risk variants for obesity, like those reported inFTO and ABCA1, have also been associated to ED disorders. The present study aimed to analysed leptin circulating levels and the interaction between obesity-risk variants in FTO and ABCA1, in adolescents diagnosed with ED. A total of 99 individuals diagnosed with ED were genotype using Taqman probes for FTO (rs9939609) and ABCA1 (p.Arg230Cys, rs9282541). Commercial enzyme-linked immunosorbent assays were utilized to determined circulating leptin. Differences in leptin concentration were analysed by t-Student or ANOVA test. Gene-gene interaction were analysed using general estimation equations. Circulating leptin levels differed between the three diagnostic groups, lead by individuals diagnosed with binge eating-disorder. In individuals with more than 3 of episodes of binge-eating per week having the highest leptin levels. Also, we found that carriers of both risk alleles had the highest leptin levels. Our observations found an interaction between FTO rs9969609 and the native American-origin ABCA1 p.Arg230Cys to modulate circulating leptin levels in Mexican adolescents diagnosed with eating-disorders.

Cortisol can be considered as one biomarker for diagnosis of suicide; nevertheless, several studies have shown conflicting results. This study aimed to evaluate the levels of cortisol in individuals with suicide behavior and controls (healthy or with other psychiatric disorders). Published articles were searched on online databases (PubMed, Scopus and EBSCO). Standardized mean differences (SMD), heterogeneity, publication bias and sensitivity were assessed using the Comprehensive Meta-Analysis (CMA) statistical software. The meta-analysis comprised 30 studies that provided 1775 cases, and 2162 controls (696 healthy individuals and 1465 individuals with other psychiatric diagnoses). The pooled results revealed that cortisol levels were higher in individuals with suicide behavior (SMD = 0.92, 95%CI = 0.26; 1.57, P = 0.006; I2 = 88%, Q

Schizophrenia (SCZ) and bipolar disorder (BD) cause similar symptomatology. A correlation between these disorders has been found. We aimed to explore shared CNVs between SCZ and BD, in 35 sibpairs diagnosed with SCZ and 21 sibpairs diagnosed with BD. CNV calling was performed using data derived of Psycharray, by PennCNV. We did not find any shared CNVs between individuals diagnosed with BD and SCZ, neither with psychotic symptoms in individuals with BD. Nevertheless, we found a significant higher CNV burden in early-onset SCZ. This is one of the first's studies analyzing shared CNVs between SCZ and BD in Mexican population.