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Medicine (Baltimore) ; 98(46): e17403, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31725603


Studies investigating the association between gene variants and depression susceptibility found inconsistent data. The present study aimed to clarify whether CNR1rs1049353, CNR1 AAT triplet repeat, and CNR2rs2501432 polymorphisms confer higher risk for depressive disorder.Literature from PubMed, Medline, Embase, Scopus, Cochrance Library, and Wanfang databases was searched (up to August 20, 2018). Seven case-control studies with various comorbidities were eligible. We targeted CNR single-nucleotide polymorphisms (SNPs) that have been reported by 2 or more studies to be involved in the current meta-analysis, resulting in a final list of 3 SNPs: CNR1rs1049353, CNR1 AAT triplet repeat polymorphism, and CNR2rs2501432. Odds ratios (ORs) and 95% confidence intervals (CIs) for allele and homozygote comparisons, dominant and recessive models, and triplet repeat polymorphism ((AAT)n≥5, ≥5 vs (AAT)n<5, <5 or <5, ≥5) were assessed using a random effect model as measures of association. Heterogeneity among included studies was analyzed using sensitivity test. Publication bias was also explored by Egger and rank correlation test.overall, no significant association was found between depression and CNR1rs1049353 (G vs A: OR [95% CI] = 1.09 [0.61-1.95]; GG vs AA: 1.29 [0.73-2.26]; GG vs GA+AA: 1.10 [0.57-2.10]; GG+GA vs AA: 1.25 [0.72-2.18]; and AAT triplet repeat polymorphism ((AAT)n≥5, ≥5 vs (AAT)n<5, <5 or <5, ≥5): 1.92 [0.59-6.27]. In contrast, a significant association between CNR2rs2501432 and depression was detected, and the ORs and 95% CIs are as follows: allele contrast (OR = 1.39, 95% CI = [1.12-1.72], P = .003); homozygous (OR = 2.19, 95% CI = [1.34-3.59], P = .002); dominant (OR = 1.93,95% CI = [1.23-3.04], P = .005); and recessive (OR = 1.41, 95% CI = [1.04-1.92], P = .03).This meta-analysis revealed that CNR1rs1049353 or AAT triplet repeat polymorphism had no association with susceptibility to depression, while CNR2rs2501432 polymorphism was a remarkable mark for depression patients.

Depressão/genética , Predisposição Genética para Doença/genética , Polimorfismo de Nucleotídeo Único , Receptor CB1 de Canabinoide/genética , Receptor CB2 de Canabinoide/genética , Alelos , Estudos de Casos e Controles , Humanos , Razão de Chances , Fatores de Risco
Psychiatry Res ; 266: 168-174, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29864617


This study evaluated the life quality of Chinese parents of preschool children with autism spectrum disorder (ASD) and their association with child social impairment and childcare burden. The participants included 406 families of children with ASD and 513 families with typically developing (TD) children. The findings indicated that parents in the ASD group had a lower quality of life than parents in the TD group, whereas only mother of children with ASD experienced a greater childcare burden than mother with TD children. Lower parental quality of life were associated with higher social impairment of children. To further clarify the correlativity of child social impairment, parental quality of life and childcare burden, the mediation analyses were conducted. The results showed that childcare burden mediated the influence of child social impairment on maternal quality of life, while it has no mediating effect on fathers. It implies that social impairment of children affects parental quality of life in different ways.

Transtorno do Espectro Autista/psicologia , Desenvolvimento Infantil , Pais/psicologia , Qualidade de Vida/psicologia , Transtornos do Comportamento Social/psicologia , Adulto , Transtorno do Espectro Autista/diagnóstico , Transtorno do Espectro Autista/epidemiologia , Criança , Pré-Escolar , China/epidemiologia , Pai/psicologia , Feminino , Humanos , Masculino , Mães/psicologia , Transtornos do Comportamento Social/diagnóstico , Transtornos do Comportamento Social/epidemiologia
BMC Psychiatry ; 18(1): 11, 2018 01 17.
Artigo em Inglês | MEDLINE | ID: mdl-29343227


BACKGROUND: Autism is a neurodevelopmental disorder with an unclear etiology. Pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) have been suggested to play a role in the etiology of autism. The current study explores the associations among maternal pre-pregnancy BMI, GWG and the risk of autism in the Han Chinese population. METHODS: Demographic information, a basic medical history and information regarding maternal pre-pregnancy and pregnancy conditions were collected from the parents of 705 Han Chinese children with autism and 2236 unrelated typically developing children. Binary logistic regressions were conducted to calculate the odds ratio (OR) for the relationship among pre-pregnancy BMI, GWG and the occurrence of autism. The interaction between pre-pregnancy BMI and GWG was analyzed by performing stratification analyses using a logistic model. RESULTS: After adjusting for the children's gender, parental age and family annual income, excessive GWG was associated with autism risk in the entire sample (OR = 1.327, 95% CI: 1.021-1.725), whereas the relationship between maternal pre-pregnancy BMI and autism was not significant. According to the stratification analyses, excessive GWG increased the risk of autism in overweight/obese mothers (OR = 2.468, 95% CI: 1.102-5.526) but not in underweight or normal weight mothers. CONCLUSIONS: The maternal pre-pregnancy BMI might not be independently associated with autism risk. However, excessive GWG might increase the autism risk of offspring of overweight and obese mothers.

Grupo com Ancestrais do Continente Asiático , Transtorno Autístico/etiologia , Índice de Massa Corporal , Obesidade , Complicações na Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ganho de Peso , Adulto , Transtorno Autístico/etnologia , Estudos de Casos e Controles , Criança , China , Feminino , Humanos , Modelos Logísticos , Razão de Chances , Sobrepeso , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etnologia , Estudos Retrospectivos , Fatores de Risco , Magreza
Schizophr Res ; 176(2-3): 259-263, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27377977


BACKGROUND: Increasing evidence shows that schizophrenia patients with long-term exposure to antipsychotic medications have decreased bone mass, which suggests that they are at a high risk of osteoporosis. However, the mechanism underlying this remains unclear. In this study, we selected two bone turnover markers to explore whether atypical antipsychotics can affect bone metabolism and identified possible influencing factors. METHODS: A total of 116 schizophrenia patients (18-40years old) participated in the study. The subjects included 31 drug-naive first-episode patients and 85 patients who had undergone atypical antipsychotic monotherapy for at least 6months. A total of 71 subjects were assigned as normal controls. Demographic and physical examination data were analyzed for all subjects. The positive and negative syndrome scale (PANSS) was used to assess psychopathology in schizophrenia patients. Levels of the bone turnover markers osteocalcin and ß-CrossLaps were measured. Serum prolactin (PRL), lipid, sex hormone, glucose, insulin, and parathyroid hormone levels were also measured. RESULTS: The serum ß-CrossLaps levels of patients who had been treated with atypical antipsychotics were higher compared with those of drug-naive first-episode patients and normal subjects. Atypical antipsychotics, schizophrenia, age, gender, and body mass index, as well as serum levels of PRL, triglyceride, high-density lipoprotein cholesterol, glucose, and testosterone, were significantly associated with serum osteocalcin and ß-CrossLaps levels. Serum insulin was only positively associated with serum osteocalcin, whereas estradiol was only negatively associated with serum ß-CrossLaps. CONCLUSION: Patients who had been treated with atypical antipsychotics had accelerated bone resorption. Our findings uncover a link between atypical antipsychotics and bone metabolism, possibly through abnormalities in glucose and lipid metabolism and insulin resistance.

Antipsicóticos/uso terapêutico , Colágeno/sangue , Osteocalcina/sangue , Fragmentos de Peptídeos/sangue , Esquizofrenia/sangue , Esquizofrenia/tratamento farmacológico , Adolescente , Adulto , Biomarcadores/sangue , Remodelação Óssea/efeitos dos fármacos , Feminino , Humanos , Modelos Lineares , Masculino , Escalas de Graduação Psiquiátrica , Adulto Jovem