Persistent Alterations in Behavior and Serotonin Activity after Recovery from Anorexia and Bulimia Nervosa<sup>a</sup>

Kaye, Walter H.

doi:10.1111/j.1749-6632.1997.tb48204.x

Cited by 27 publications

(12 citation statements)

References 117 publications

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“…27 Depression and anxiety are often present before, during, and post-AN. [28][29][30] One study showed that the antidepressant serotonin and noradrenalin reuptake inhibitor, venlafaxine, may be beneficial for patients with atypical AN 31 in which weight remains just above the diagnostic threshold for AN or amenorrhoea is absent. 1 Low CSF and blood noradrenalin levels observed in long-term weight-restored AN patients compared to normals 12,13 may be explained by increased MAOA activity which would integrate well with our finding of association of AN-R with MAOA-L as this variant results in increased MAOA activity.…”

Section: Discussionmentioning

confidence: 99%

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

et al. 2003

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We earlier found an association between anorexia nervosa (AN) restrictive subtype (AN-R) and an inserted sequence within the NETpPR, a polymorphic region located in the promoter of the solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 (SLC6A2) gene. To further examine the noradrenergic system in AN-R we performed an association study with a functional polymorphism (MAOAuVNTR) in the promoter of the monoamine oxidase A (MAOA) gene. Since monoamine oxidase A metabolises noradrenalin, a positive association with the MAOA gene would be biologically plausible. The transmission disequilibrium test and 95 trios/duos (AN-R females þ biological parents) showed the main effect of the longer, more transcriptionally active form of the MAOA-uVNTR (MAOA-L) to be statistically non-significant (McNemar's v 2 ¼ 1.4, df ¼ 1, P ¼ 0.238, odds ratio: 1.4, 95% CI 0.8 -2.7). A case-control approach supported this finding. We then stratified the MAOA-uVNTR TDT data according to the (a) NETpPR genotype of the AN-R females, and (b) NETpPR allele transmitted from NETpPR-S4/L4 heterozygous mothers. In both cases, contingency table analysis revealed previously unreported genegene interaction between the MAOA and SLC6A2 genes (P ¼ 0.019 and 0.019, respectively). Receiving an MAOA-L allele more than doubles the risk for developing AN-R, conditional on an individual also being a NETpPR-L4 homozygote (stratum-specific odds ratio: 2.4, 95% CI 1.1-6.0). These results suggest important involvement of the noradrenergic system in the biological underpinnings of AN-R.

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Section: Discussionmentioning

confidence: 99%

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

et al. 2003

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“…Contudo, o maior metabólito da 5-HT encontra-se diminuído em pacientes com AN. [22][23][24] É bem reconhecido que a administração de agentes serotoninérgicos em animais e pessoas sem transtornos alimentares suprime o comportamento alimentar (velocidade do ato de se alimentar e tamanho das refeições), particularmente, diminuindo a ingestão de carboidratos. 25 Esses efeitos da 5-HT podem ser resumidos como uma intensificação da saciedade após o inicio do comportamento consumatório de alimento.…”

Section: Somáticosunclassified

“…22,27,28 Assim, um fator predisponente no desenvolvimento da BN seria a menor atividade de sistemas associados à 5-HT cerebral.…”

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Etiologia dos transtornos alimentares: aspectos biológicos, psicológicos e sócio-culturais

Morgan

Vecchiatti

Negrão

2002

Rev. Bras. Psiquiatr.

105

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Os transtornos alimentares possuem uma etiologia multifatorial, composta de predisposições genéticas, socioculturais e vulnerabilidades biológicas e psicológicas. Entre os fatores predisponentes, destacam-se a história de transtorno alimentar e (ou) transtorno do humor na família, os padrões de interação presentes no ambiente familiar, o contexto sociocultural, caracterizado pela extrema valorização do corpo magro, disfunções no metabolismo das monoaminas centrais e traços de personalidade. A dieta é o comportamento precursor que geralmente antecede a instalação de um transtorno alimentar. Contudo, a presença isolada da dieta não é suficiente para desencadear o transtorno alimentar, tornando-se necessária uma interação entre os fatores de risco e outros eventos precipitantes. Por último, o curso transitório ou crônico de um transtorno alimentar está relacionado à persistência de distorções cognitivas, à ocorrência de eventos vitais significativos e a alterações secundárias ao estado de desnutrição. Resumo Descritores Abstract Keywords IntroduçãoOs transtornos alimentares (TA) têm uma etiologia multifatorial, ou seja, são determinados por uma diversidade de fatores que interagem entre si de modo complexo, para produzir e, muitas vezes, perpetuar a doença. Classicamente, distinguem-se os fatores predisponentes, precipitantes e os mantenedores dos TA.

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“…2 Trait-related abnormalities in the serotonergic system have also been observed in subjects recovered from anorexia nervosa. 3 The A allele of the −1438 G/A polymorphism in HTR2A has been implicated as a vulnerability allele for anorexia nervosa in four case-control association studies. [4][5][6][7] On the other hand, the publication of three negative association studies [8][9][10] and current absence of evidence for linkage based on the transmission disequilibrium test (TDT) in 50 family trios 8 raise the possibilities of a false positive finding, a minor effect that is difficult to detect in small samples, and the effect of clinical and/or genetic heterogeneity.…”

Section: Introductionmentioning

confidence: 99%

The 5-HT2A −1438G/A polymorphism in anorexia nervosa: a combined analysis of 316 trios from six European centres

et al. 2002

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Keywords: eating disorder; serotonin; TDT (transmission disequilibrium test); QTL (quantitative trait loci)Several case-control association studies have raised the possibility that the A allele of a −1438 G/A polymorphism in the type 2A serotonin receptor (HTR2A) gene may be a risk factor for anorexia nervosa. However the absence of linkage and the existence of negative association studies raise the possibility of false positive findings, resulting from population stratification or lack of statistical power. To address this controversy we recruited a sample of 316 patients with anorexia nervosa from six European centres, and utilised a family-based transmission disequilibrium (TDT) approach to analyse the HTR2A-1438 G/A polymorphism. Age at onset and minimal BMI were also taken into consideration in order to detect clinical heterogeneity or a quantitative trait effect. The TDT approach showed that the A allele was transmitted 133 times and not transmitted 148 times (McNemar 2 = 0.29, df = 1, P = 0.59). Also, the haplotypebased haplotype relative risk method showed no evidence for association of the A allele, in samples from each centre ( 2 Ͻ 2.15, df = 1, P Ͼ 0.14) and in the total sample ( 2 = 0.55, df = 1; P = 0.46). Furthermore, we found no evidence for heterogeneity of the A allele frequency between samples ( 2 = 2.54, df = 4, P = 0.64), either according to minimal-BMI (F1/242 = 2.14, P = 0.45) or age at onset (F1/224 = 2.39; P = 0.12). QTL-TDT analyses also showed no direct role of the A allele on these traits. We thus found no evidence for a significant role of the 5-HT 2A gene in anorexia nervosa. Previous results may have been exposed to stratification bias (which we controlled by the TDT method) and/or the risk of type 1 error (from which we were less exposed because of the sample size). Molecular Psychiatry (2002) 7, 90-94.

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Persistent Alterations in Behavior and Serotonin Activity after Recovery from Anorexia and Bulimia Nervosa^a

Cited by 27 publications

References 117 publications

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

Etiologia dos transtornos alimentares: aspectos biológicos, psicológicos e sócio-culturais

The 5-HT2A −1438G/A polymorphism in anorexia nervosa: a combined analysis of 316 trios from six European centres

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Persistent Alterations in Behavior and Serotonin Activity after Recovery from Anorexia and Bulimia Nervosaa

Cited by 27 publications

References 117 publications

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

Gene-gene interaction between the monoamine oxidase A gene and solute carrier family 6 (neurotransmitter transporter, noradrenalin) member 2 gene in anorexia nervosa (restrictive subtype)

Etiologia dos transtornos alimentares: aspectos biológicos, psicológicos e sócio-culturais

The 5-HT2A −1438G/A polymorphism in anorexia nervosa: a combined analysis of 316 trios from six European centres

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Persistent Alterations in Behavior and Serotonin Activity after Recovery from Anorexia and Bulimia Nervosa^a