Predictors of late menarche and adult height in children with anorexia nervosa

Roze, Catherine; Doyen, Catherine; Heuzey, Marie-France Le; Armoogum, Priscilla; Mouren, Marie–Christine; Léger, Juliane

doi:10.1111/j.1365-2265.2007.02912.x

Cited by 46 publications

(26 citation statements)

References 36 publications

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“…High levels of androgens during the prenatal period were reported as a possible risk factor for autistic-like disorders and later onset of puberty [139], but this finding remains under question [140]. All psychological conditions leading to malnutrition, such as anorexia nervosa [141], affect AAM due to low leptin levels that results in impaired secretion of GnRH [142]. …”

Section: Resultsmentioning

confidence: 99%

Nongenetic Determinants of Age at Menarche: A Systematic Review

Yermachenko

Dvornyk

2014

BioMed Research International

153

141

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Background. The acceleration of pubertal development is an important medical and social problem, as it may result in increased morbidity and mortality in later life. This systematic review summarizes relevant data about nongenetic factors, which contribute to age at menarche (AAM), and suggests those which may be the most important. Methods. The available literature from 1980 till July 2013 was searched using PubMed and Google Scholar databases. Finally, 154 papers were selected for the analysis. Results. Environmental factors, which may affect AAM, vary in populations of different ethnicity. The prenatal, infancy, and early childhood periods are the most susceptible to these factors. Body weight, high animal protein intake, family stressors (e.g., single parenting), and physical activity seem to influence AAM in most populations. Conclusions. The data about influence of nongenetic factors on AAM are still inconsistent. The factors affecting prenatal and early childhood growth seem to have a larger effect on further sexual maturation. Further studies are needed in order to validate the association between other environmental determinants and AAM in different ethnical groups.

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Section: Resultsmentioning

confidence: 99%

Nongenetic Determinants of Age at Menarche: A Systematic Review

Yermachenko

Dvornyk

2014

BioMed Research International

153

141

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“…The general lack of support for pubertal effects on AN may be due to the relatively small number of studies conducted and/or the difficulty of studying early-onset AN that has a much lower prevalence (i.e., .5%) than BN (i.e., 1-3%) or EDNOS (i.e., ~10%) (American Psychiatric Association, 2000). In addition, because extreme dieting frequently begins months/years before AN onset and can forestall pubertal development (Lantzouni et al, 2002; Roze et al, 2007), disentangling the effects of the disorder on puberty versus the effects of puberty on the disorder can be difficult. This tends to be less of an issue for BN and EDNOS where the dieting is less extreme and other core symptoms (e.g., binge eating, purging) tend not to disrupt pubertal processes.…”

Section: Associations Between Pubertal Status Pubertal Timing and Ementioning

confidence: 99%

Puberty as a critical risk period for eating disorders: A review of human and animal studies

Klump

2013

Hormones and Behavior

246

183

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Puberty is one of the most frequently discussed risk periods for the development of eating disorders. Prevailing theories propose environmentally mediated sources of risk arising from the psychosocial effects (e.g., increased body dissatisfaction, decreased self-esteem) of pubertal development in girls. However, recent research highlights the potential role of ovarian hormones in phenotypic and genetic risk for eating disorders during puberty. The goal of this paper is to review data from human and animal studies in support of puberty as a critical risk period for eating disorders and evaluate the evidence for hormonal contributions. Data are consistent in suggesting that both pubertal status and pubertal timing significantly impact risk for most eating disorders in girls, such that advanced pubertal development and early pubertal timing are associated with increased rates of eating disorders and their symptoms in both cross-sectional and longitudinal research. Findings in boys have been much less consistent and suggest a smaller role for puberty in risk for eating disorders in boys. Twin and animal studies indicate that at least part of the female-specific risk is due to genetic factors associated with estrogen activation at puberty. In conclusion, data thus far support a role for puberty in risk for eating disorders and highlight the need for additional human and animal studies of hormonal and genetic risk for eating disorders during puberty.

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“…However, data are conflicting in young women with AN with studies variably reporting shorter, comparable or taller stature compared to peers (22–24). This dichotomy between the sexes may relate to the fact that much of statural growth is complete at the time of AN onset in girls, given the earlier growth spurt and cessation of statural growth in girls compared with boys.…”

Section: Growth Hormone (Gh)- Insulin Like Growth Factor-1 (Igf-1) Axismentioning

confidence: 99%

“…Furthermore, peripheral levels of oxytocin (which is anorexigenic) are also appropriately lower in AN (75). Insulin, amylin and oxytocin are bone anabolic, and reductions in these hormones in AN are associated with low bone density 24,64,65 .…”

Section: Other Hormonesmentioning

confidence: 99%

Anorexia Nervosa and Its Associated Endocrinopathy in Young People

Misra

Klibanski

2016

Horm Res Paediatr

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Anorexia nervosa (AN) is a condition of severe undernutrition associated with adaptive changes in many endocrine axes. These changes include hypogonadotropic hypogonadism, acquired growth hormone resistance with low insulin-like growth factor 1 (IGF-1) levels, hypercortisolemia, altered secretion of adipokines and appetite-regulating hormones, and low bone mineral density (BMD). Bone health is impaired subsequent to a low body mass index, decreased lean mass, and the endocrine changes described above. In addition to low areal BMD, AN is characterized by a decrease in volumetric BMD, changes in bone geometry, and reductions in strength estimates, leading to an increased risk for fracture. Weight restoration is essential for restoration of normal endocrine function; however, hypercortisolemia, high peptide YY levels, and ghrelin dynamics may not completely normalize. In some patients, hypogonadotropic hypogonadism persists despite weight restoration. Weight gain and menstrual recovery are critical for improving bone health in AN; however, residual deficits may persist. Physiologic estrogen replacement using transdermal, but not oral, estrogen increases bone accrual in adolescents with AN, while bisphosphonates improve BMD in adults. Recombinant human IGF-1 and teriparatide have been used in a few studies as bone anabolic therapies. More data are necessary to determine the optimal therapeutic strategies for low BMD in AN.

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Predictors of late menarche and adult height in children with anorexia nervosa

Abstract: The intensity of the disease affects the timing of menarche but not adult height in most patients. Hospitalization, despite often being an effective means of managing AN, does not reduce the impact of AN on growth.

Cited by 46 publications

References 36 publications

Nongenetic Determinants of Age at Menarche: A Systematic Review

Nongenetic Determinants of Age at Menarche: A Systematic Review

Puberty as a critical risk period for eating disorders: A review of human and animal studies

Anorexia Nervosa and Its Associated Endocrinopathy in Young People

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