scholarly journals The Impact of the Serotonin Transporter Gene Promoter DNA Methylation on Anorexia Nervosa:A Preliminary Longitudinal Study

Author(s):  
Jue Chen ◽  
Zeping Xiao ◽  
Qianqian He ◽  
Qing Kang ◽  
Shunying Yu ◽  
...  

Abstract BackgroudThe serotonin system has been reported to be involved in the pathogenesis of anorexia nervosa (AN). The promoter region of serotonin transporter gene (SLC6A4), also called 5-HTTLPR, responsible for serotonin reuptake, has received much attention, especially 5-HTTLPR methylation, which was associated with abnormal eating behaviors. The study was aimed to explore the association between 5-HTTLPR methylation and AN, as well as its predictive effect on therapeutic response.Methods91 AN patients and 87 healthy controls (HCs) were recruited. Only 30 patients completed the 12-week follow-up. 5-HTTLPR methylation levels and clinical symptoms were assessed at baseline for all participants, at the fourth and the twelfth week for follow-up patients. 5-HTTLPR methylation was measured by MassArray methods and clinical symptoms were mainly evaluated by the EDE-Q6.0 scale. ResultsAN patients had higher methylation at CpG 11, CpG 24.25, CpG 31.32 and CpG_mean than healthy controls (P=0.039, 0.042, 0.018, 0.001). Furthermore, it was the binge/purging subtype that revealed significant hypermethylation at CpG4 and CpG_mean (P=0.027, 0.031). However, it failed to discover significant differences between AN-R and AN-BP groups at all units. Besides, CpG 11 methylation level was positively correlated with EDEQ-6.0 total score in patients (r=0.226, P=0.047). The methylation level of CpG11, CpG26.27.28, CpG31.32, CpG33.34.35.36 and CpG_mean decreased after treatment, but not significantly. 5-HTTLPR methylation was not significantly different between the two groups after treatment.ConclusionsOur study provided preliminary evidence that 5-HTTLPR methylation played vital roles in AN pathogenesis. The characteristic of 5-HTTLPR among untreated AN patients was hypermethylation. However, whether it is the biomarker to distinguish the subtypes and therapeutic response of AN needs further investigation.

2020 ◽  
Author(s):  
Andrea Bonassi ◽  
Ilaria Cataldo ◽  
Giulio Gabrieli ◽  
Moses Tandiono ◽  
Jia Nee Foo ◽  
...  

Human social interactions ensure recognition and approval from others, both in offline and online environments. This study applies a model from behavioural genetics on Instagram sociability to explore the impact of individual development on the behaviour on social networks.We hypothesize that sociable attitudes on Instagram resulted from an interaction between serotonin transporter gene alleles and the individual’s social relationship with caregivers. We assess environmental and genetic components of 57 Instagram users. The self-report questionnaire Parental Bonding Instrument is adopted to determine the quality of parental bonding. The number of posts, followed users (“followings”), and followers are collected from Instagram as measures of online social activity. Additionally, the ratio between the number of followers and followings (“Social Desirability Index”) was calculated to estimate the asymmetry of each user’s social network. Finally, buccal mucosa cell samples were acquired, and the polymorphism rs25531 (T/T homozygotes vs C-carriers) within the serotonin transporter gene was examined.In the preliminary analysis, we identified a gender effect on the number of followings. In line with our predictions, we specifically found a gene- environment interaction on the standardized Instagram “Social Desirability Index”: users with the genotype more sensitive to environmental influences (T/T homozygotes) showed a higher Instagram “Social Desirability Index” than non-sensitive ones (C-carriers) when they experienced positive maternal care.This result may contribute to the understanding of online social behaviour from a gene*environment perspective.


2012 ◽  
Vol 159B (5) ◽  
pp. 491-500 ◽  
Author(s):  
Giovanni Castellini ◽  
Valdo Ricca ◽  
Lorenzo Lelli ◽  
Silvia Bagnoli ◽  
Ersilia Lucenteforte ◽  
...  

2012 ◽  
Vol 3 ◽  
Author(s):  
Nassima Ait-Daoud ◽  
Chamindi Seneviratne ◽  
Justin B. Smith ◽  
John D. Roache ◽  
Michael A. Dawes ◽  
...  

2018 ◽  
Vol 2 (1) ◽  
pp. 8-15 ◽  
Author(s):  
Ki Park ◽  
Eric Egelund ◽  
Tianyao Huo ◽  
C. Noel Bairey Merz ◽  
Eileen M. Handberg ◽  
...  

Introduction: Association of serotonin transporter gene ( 5-HTTLPR) polymorphisms with adverse cardiovascular (CV) events in women with suspected ischemia has not yet been reported. We hypothesized an association of 5-HTTLPR polymorphisms with risk of adverse CV events in women with suspected ischemic heart disease (IHD) referred for coronary angiography enrolled in the Women’s Ischemia Syndrome Evaluation (WISE). Method: We studied clinical and angiographic data and DNA from a cohort of 437 Caucasian women enrolled in the WISE genotyped for the long (L) and short (S) variant of the 5-HTTLPR polymorphism. Women were followed yearly for adverse CV events (defined as first occurrence of all-cause death, myocardial infarction, stroke, or heart failure hospitalization) with data collected at WISE 10-year follow-up. Exploratory analyses compared outcomes between genotype groups. Results: A total of 437 women, with baseline, angiographic, and long-term follow-up data, were successfully genotyped. Their mean age was 58 ± 11 years and body mass index 29 ± 6; 54% had hypertension, 18% diabetes, 50% dyslipidemia, 20% depression history, and only 34% had obstructive CAD. At 8.9 years median follow-up, the SS genotype was associated with significantly increased risk of adverse CV event versus LL + LS (1.93, confidence interval [CI]: 1.03-3.61, P = .03). Results were not significant for all-cause death (hazard ratio: 1.63, CI: 0.91-2.93, P = .09). Conclusion: Among a cohort of Caucasian women with suspected IHD enrolled in the WISE, the SS homozygous genotype for the 5-HTTLPR polymorphism was associated with increased risk of adverse CV outcomes.


Author(s):  
Leandra Kuhn ◽  
Hannes Noack ◽  
Nadine Skoluda ◽  
Lisa Wagels ◽  
Ann-Kristin Röhr ◽  
...  

AbstractThe experience of stress is related to individual wellbeing and vulnerability to psychopathology. Therefore, understanding the determinants of individual differences in stress reactivity is of great concern from a clinical perspective. The functional promotor polymorphism of the serotonin transporter gene (5-HTTLPR/rs25531) is such a factor, which has been linked to the acute stress response as well as the adverse effect of life stressors. In the present study, we compared the impact of two different stress induction protocols (Maastricht Acute Stress Test and ScanSTRESS) and the respective control conditions on affective ratings, salivary cortisol levels and cognitive performance. To this end, 156 healthy young males were tested and genotyped for the 5-HTTLPR/rs25531 polymorphism. While combined physiological and psychological stress in the MAST led to a greater cortisol increase compared to control conditions as well as the psychosocial ScanSTRESS, subjective stress ratings were highest in the ScanSTRESS condition. Stress induction in general affected working memory capacity but not response inhibition. Subjective stress was also influenced by 5-HTTLPR/rs25531 genotype with the high expression group showing lower stress ratings than lower expression groups. In line with previous research, we identified the low expression variant of the serotonin transporter gene as a risk factor for increased stress reactivity. While some dimensions of the human stress response may be stressor specific, cognitive outcomes such as working memory performance are influenced by stress in general. Different pathways of stress processing and possible underlying mechanisms are discussed.


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