Decreased whole-blood global DNA methylation is related to serum hormones in anorexia nervosa adolescents

Tremolizzo, Lucio; Conti, Elisa; Bomba, Monica; Uccellini, Orlando; Rossi, Maria Sara; Marfone, M; Corbetta, F; Santarone, Mauro; Raggi, Maria Elisabetta; Neri, Francesca; Ferrarese, Carlo; Nacinovich, Renata

doi:10.3109/15622975.2013.860467

Cited by 38 publications

(32 citation statements)

References 48 publications

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“…AN and BN subjects showed increased methylation of dopamine system genes [103]. Taken together, these findings suggest that alterations in DNA methylation can lead to EDs by influencing a wide variety of systems implicated in behavioral/affective regulation, sensitivity to nutritional insufficiencies, and body-weight maintenance [99,104,105]. Genome-wide methylation profiles in women with AN-restrictive type, and women with AN-binge/purge type compared with normal-weight/normal-eater control women, showed higher and less variable global methylation patterns in AN than controls [59].…”

Section: Epigeneticsmentioning

confidence: 75%

An Evolutionary Genetic Perspective of Eating Disorders

Mayhew

Pigeyre

Couturier³

et al. 2017

Neuroendocrinology

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Eating disorders (ED) including anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) affect up to 5% of the population in Western countries. Risk factors for developing an ED include personality traits, family environment, gender, age, ethnicity, and culture. Despite being moderately to highly heritable with estimates ranging from 28 to 83%, no genetic risk factors have been conclusively identified. Our objective was to explore evolutionary theories of EDs to provide a new perspective on research into novel biological mechanisms and genetic causes of EDs. We developed a framework that explains the possible interactions between genetic risk and cultural influences in the development of ED. The framework includes three genetic predisposition categories (people with mainly AN restrictive gene variants, people with mainly BED variants, and people with gene variants predisposing to both diseases) and a binary variable of either the presence or absence of pressure to be thin. We propose novel theories to explain the overlapping characteristics of the subtypes of AN (binge/purge and restrictive), BN, and BED. For instance, mutations/structural gene variants in the same gene causing opposite effects or mutations in nearby genes resulting in partial disequilibrium for the genes causing AN (restrictive) and BED may explain the overlap of phenotypes seen in AN (binge/purge).

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Section: Epigeneticsmentioning

confidence: 75%

An Evolutionary Genetic Perspective of Eating Disorders

Mayhew

Pigeyre

Couturier³

et al. 2017

Neuroendocrinology

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“…Epigenetic studies also suffer from power issues as candidate gene studies have in detecting reproducible associations. For example, while Tremolizzo et al (Tremolizzo et al, 2014) identified a modest yet significant reduction of global DNA methylation in AN, Saffrey et al (Saffrey et al, 2014) reported no alterations in global or gene-specific DNA methylation. Yet, a most recent study by Booij et al reported a higher global DNA methylation in AN groups compared to controls (Booij et al, 2015).…”

Section: Alteration Of Gene Expression: Mrna and Methylationmentioning

confidence: 99%

Contemporary views on the genetics of anorexia nervosa

Shih

Woodside

2016

European Neuropsychopharmacology

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Anorexia nervosa (AN) is a serious mental illness characterized by severe dietary restriction that leads to high rates of morbidity, chronicity, and mortality. Unfortunately, effective treatment is lacking and few options are available. High rates of familial aggregation and significant heritability suggested that the complex etiology of AN is affected by both genetic and environmental factors. In this paper, we review studies that reported common and rare genetic variation that influence susceptibility of AN through candidate gene studies, genome-wide association studies, and sequencing-based studies. We also discuss gene expression, methylation, imaging genetics, and pharmacogenetics to demonstrate that these studies have collectively advanced our knowledge of how genetic variation contributes to AN susceptibility and clinical course. Lastly, we highlight the importance of gene by environment interactions (G x E) and share our enthusiasm for the use of nutritional genomic approaches to elucidate the interaction among nutrients, metabolic intermediates, and genetic variation in AN. A deeper understanding of how nutrition alters genome stability, how genetic variation influences uptake and metabolism of nutrients, and how response to food components affects disordered eating, will lead to personalized dietary interventions and effective nutraceutical and pharmacological treatments for AN.

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“…Blood samples were collected between 8.00 and 8.30 a.m., following overnight fasting and plasma fractions were immediately obtained, as previously described [13]. Whole blood for DNA extraction and plasma aliquots were stored at -80°C until assay.…”

Section: Methodsmentioning

confidence: 99%

“…Whole blood for DNA extraction and plasma aliquots were stored at -80°C until assay. Hcy determination was performed only in AN patients and blood samples were kept on ice before immediate assay by HPLC at the Laboratory of Analysis of the San Gerardo Hospital that gave reference values as well [13]. Laboratory investigations were carried out blindly with respect to clinical data.…”

Section: Methodsmentioning

confidence: 99%

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Beta-Amyloid Plasma Levels in Adolescents with Anorexia Nervosa of the Restrictive Type

Conti¹,

Nacinovich²,

Bomba³

et al. 2015

Neuropsychobiology

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Background: Reduced plasma leptin and elevated homocysteine (Hcy) are known to lead to increased β-amyloid (Aβ) production, besides being hallmarks of anorexia nervosa (AN) of the restrictive type. AN subjects display several neuropsychiatric manifestations, which may entail Aβ-mediated altered synaptic functions. The aim of this study consisted in assessing Aβ plasma levels in AN patients. Methods: A total of 24 adolescent female AN outpatients were recruited together with 12 age-comparable healthy controls. For each subject we assessed Aβ40 and leptin plasma levels, as well as APOE genotype. Hcy plasma levels were also determined in AN patients who underwent clinical characterization, including the Eating Disorder Inventory-3 (EDI-3), the Children's Depression Inventory (CDI) and the estimation of the speed of BMI loss (DPI, disease progression index). Results: Plasma Aβ40 levels were similar between patients and controls, while a marked reduction was observed for leptin (∼80%) in AN patients. Aβ40 plasma levels failed to correlate with leptin, while a linear correlation was present with Hcy (r = 0.50, p < 0.03). Examined clinical features were not related with Aβ40 plasma levels, with the only exception of the DPI (r = 0.47, p < 0.03). Conclusion: This exploratory study does not support a significant role for altered Aβ production in AN-associated dysfunctions. Further studies are required to clarify whether exceptions to this conclusion can be drawn for those patients expressing significantly elevated Hcy plasma levels or for those progressing more rapidly.

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Decreased whole-blood global DNA methylation is related to serum hormones in anorexia nervosa adolescents

Abstract: A better definition of the epigenetic dysregulation underlying AN pathology or vulnerability might lead to develop useful markers for diagnosis, prognostic classification and tailored therapeutic interventions in these vulnerable patients since the earliest phases of their disease.

Cited by 38 publications

References 48 publications

An Evolutionary Genetic Perspective of Eating Disorders

An Evolutionary Genetic Perspective of Eating Disorders

Contemporary views on the genetics of anorexia nervosa

Beta-Amyloid Plasma Levels in Adolescents with Anorexia Nervosa of the Restrictive Type

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