This study presents the effect of MDR1 gene polymorphisms on sexual function in 18 women with bulimia nervosa, 18 women with anxiety disorders, and 19 healthy control subjects.
P-adiponectin was elevated in patients with BN at baseline and at follow-up when compared to patients without BN and controls (P<0.004 and <0.008 respectively).
AGRPrs13338499 polymorphism was associated with lowest illness-related BMI in those with AN (p = 0.0013), and NTRK2 rs1042571 was associated with highest BMI in those with BN (p = 0.0018).
Three of the GWS loci identified (rs200889048, rs12490016 and rs1630623) were not previously reported by GWAS of BMI in the general population, and two of them raise interesting hypotheses: rs12490016-a regulatory variant located within LINC00880, where there are other GWAS-identified variants associated with birth size, adiposity in newborns and bulimia symptoms, which also interact with social stress in relation to birth size; rs1630623-a regulatory variant related to ALDH1A1, a gene involved in alcohol metabolism and adipocyte plasticity.
The current results implicate the following genes: CLEC5A, LOC136242, TSHZ1, and SYTL5 for the AN spectrum phenotype; NT5C1B for the BN spectrum phenotype; and ATP8A2 for the disordered eating behaviors phenotype.
These results suggest that the 196G/A SNP of the human BDNF gene does not contribute to the genetic susceptibility to BN and BED, but may predispose those patients to a more severe binge eating behavior.
We observed a significant site×group (BN vs. NE) interaction indicating that women with BN showed increases in methylation at specific regions of the BDNF promoter.
This study: (1) assessed the role of leptin, melanocortin, and neurotrophin genetic variants in conferring risk for AN and BN; and (2) explored the involvement of these genes in body mass index (BMI) variations within AN and BN.
We have found that the Met66 variant is strongly associated to all ED subtypes (AN, ANR, binge-eating/purging AN and BN), and that the -270C BDNF variant has an effect on BN and late age at onset of weight loss.
Several lines of evidence support that brain-derived neurotrophic factor (BDNF) plays an essential role in eating behaviour and that alterations on this neurotrophic system participates in the susceptibility to both AN and BN.
Our data strongly suggest that altered BDNF levels modulated by BDNF gene variability are associated with the susceptibility to ED, providing physiological evidence that BDNF plays a role in the development of AN and BN, and strongly arguing for its involvement in eating behavior and body weight regulation.
Balanced sporting activity should be considered a resource in the treatment of eating disorders (ED), in particular of the BED and in obesity but also, if conducted and guided by expert preparers and rehabilitators, in some forms of anorexia and in bulimia.</p> Objective: However, when physical activity becomes compulsive, an end in itself and which interferes predominantly in daily activities, aimed essentially at energy consumption to force weight loss up to marked decay, it becomes a pathological instrument, an elimination course, a form purging and falls within the diagnostic criteria in bulimia and anorexia nervosa.
The 2012-2013 National Epidemiologic Survey on Alcohol and Related Conditions-III (N=36,309) included respondents who met the criteria for specific lifetime DSM-5 EDs and answered questions regarding help-seeking for their ED symptoms (anorexia nervosa [AN]: n=275; bulimia nervosa [BN]: n=91; and binge-eating disorder [BED]: n=256).
Inclusion criteria were: 1) full text available in English; 2) published in a peerreviewed journal and using the following keywords: neurotransmitters (AgRP, BDNF, αMSH, NP Y, endocannabinoids, adiponectin, CCK, ghrelin, GLP-1, insulin, leptin, PP, PYY), hormones (FSH, LH, estrogen, progesterone, testosterone) and bulimia nervosa, eating disorders.
Women seeking treatment for BN (N=129) and non-eating-disordered comparison women (N=98) provided blood samples for assays of the Bcl1 polymorphism, and completed structured interviews assessing eating symptoms, psychiatric symptoms and childhood abuse.
The measurement of 5-HT1A receptors in drug-naïve schizophrenic patients using the in vivo PET methodology revealed an increase of cortical 5-HT1A receptor binding potential in schizophrenia. beta-CIT as a ligand for measurement of 5-HT transporter densities (5-HTT) revealed lower rates in depression compared to age- and sex-matching healthy controls, a measurement that has also been obtained for bulimia.
The 3111T/C polymorphism of the CLOCK gene confers a predisposition to a lifetime lower body weight in patients with anorexia nervosa and bulimia nervosa: a preliminary study.
These findings, although preliminary, suggest that the 3111T/C polymorphism of the CLOCK gene does not play a major role in the genetic vulnerability to AN and BN, but it seems to predispose eating disorders (EDs) patients to a more severe lifetime body weight loss.
We found significantly higher levels of CB(1) receptor mRNA in the blood of patients with AN (DeltaCT: -3.9 (1.0); KW: 11.31; P=0.003) and BN (DeltaCT: -3.7 (1.7)) when compared to controls (DeltaCT: -4.6 (0.6); Dunn's test AN vs.