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Menopause Live - IMS Updates
InFocus

Date of release: 20 June, 2016

Eating disorders in midlife women

Eating disorders afflict women across their lifespan with peak onset during critical and sensitive development periods or reproductive hormone changes, such as puberty. A growing body of research supports the role of reproductive hormones, specifically estrogen, in the risk for eating disorders and related symptomatology in adolescence and young adulthood. Like puberty, perimenopause is characterized by estrogen change and may also present a window of vulnerability to development of eating disorders. In a recent paper by Baker and Runfola, the evidence is discussed that suggests perimenopause may indeed be a vulnerable period for the development or redevelopment of an eating disorder for midlife women [1]. Drawing from what is known about the influence of estrogen on eating disorders at younger ages and from other psychiatric disorders with similar risk trajectories (e.g. perimenopausal depression), a potential mechanism of risk for a perimenopausal eating disorder is described and how this can be explored in future research. Investigating vulnerability to perimenopausal eating disorders will clarify the etiology of eating disorders, identify reproductive stage-specific risk profiles, and guide future treatment directions.

Comment

Baker and Runfola conducted a comprehensive search of PubMed for articles published in the area of midlife eating disorders (EDs) as well as the hormonal etiology of EDs and other psychiatric disorders [1]. Eating disorders are erroneously stereotyped as a disease of adolescents and young adulthood. At the onset of puberty, critical body mass and adipose tissue are required for the menarche occurrence. The physiological regulation of food intake is a complex homeostatic process that is regulated by many metabolic factors. Midlife eating disorders may be detrimental due to the body’s lessened ability to fight disease and physical insult. Adipose tissue, as a ‛third ovary’, has many protective roles. Perimenopause, climacterium, or the menopause transition, may be a significant period of vulnerability for the development, exacerbation, or relapse of ED symptoms. ED in women aged 40-60 is significantly higher in perimenopausal women than in women of reproductive age [2]. Visceral fat increases by 400% in women between the third and seventh decade [3]. The type of the visceral fat tissue surrounding the myocardium and epicardium can be a new risk factor for cardiovascular disorders. Differentiation of pre-adypocyte to adipocyte is induced by nutritents, hormones (insulin, glucocorticoids, insulin-like growth factor-1), paracrine and autocrine effectors (cAMP, free fatty acids). This complex mechanism is under hypothalamic satiety center control (neuropeptides, leptin, insulin), sympathetic nervous system (energy expenditure, lipolysis), gastrointestinal system (more than 40 hormones including ghrelin, peptid YY, leptin, adiponectin, resistin, tissue necrosis factor α, etc.) and n. arcuatus, paraventricularis, vagus and tractus solitarius. During aging, there is inability to keep key adipogenic regulators. Changes in expression of c/EBPα, β and δ are involved in transactivations of adipose specific genes including adiponectin, leptin, GLUT4 and fat acids. Hypothalamus programming of systemic aging involving IKK-β, NF-κB and GnRH are involved during puberty and climacterium [4]. At the beginning of the climacteric period, estradiol is high, it fluctuates, and in the late phases it drops, inducing many other changes. It seems that biology tries to protect women, partly by weak estrogens (estrone, etc.) from adipose tissue, increasing weight by 5 kg approximately.

So, the authors of this study indicate that risk for eating disorder symptoms at perimenopause may, in part, be due to the changes in estrogen levels. Menopause onset is clearly associated with decreased estrogen and fat oxidation that can predispose to obesity if lifestyle changes are not made [5]. The authors hypothesize that women with perimenopausal EDs represent a subgroup of women who are hypersensitive to fluctuations in estrogen or who react strongly to the effects of varying estrogen. They may represent a hormone-sensitive ED phenotype. They can have genetically determined higher receptor sensitivity, or some other hormonal changes can influence their estrogen receptor sensitivity. Abdominal obesity links insulin resistance, dyslipidemia, diabetes, hypertension, gynecological cancers, venous thromboembolism, and osteoarthritis, increasing morbidity and mortality [6]. About 44% of postmenopausal women are overweight among whom 23% are obese [7]. Thus estrogen administration could be beneficial for those groups of women and could ameliorate co-morbidities. It is most important to start with estrogen therapy during the climacterium and prevent further increase in weight. Obese women seeking hormone therapy should be evaluated for their individual baseline risk.

To conclude, the study of Baker and Runfola focuses our attention on the importance of searching for a hormone-sensitive eating disorder phenotype in women and help them with the initiation of estrogen therapy on time. This is the way to improve their quality of life and decrease the morbidity and mortality rate.

Comentario

Svetlana Vujovic


Medical Faculty, University of Belgrade, Clinic of Endocrinology, Diabetes and Diseases of Metabolism, Clinical Center of Serbia, Belgrade, Serbia; President of the Serbian Menopause Society



    References

  1. Baker JH, Runfola CD. Eating disorders in midlife women: A perimenopausal eating disorder? Maturitas 2016;85:112-16


    http://www.ncbi.nlm.nih.gov/pubmed/26857889

  2. Mangweth-Matzek B, Hoek HW, Rupp CI, et al. The menopausal transition – a possible window of vulnerability for eating pathology. Int J Eat Disord 2013;46:609-16


    http://www.ncbi.nlm.nih.gov/pubmed/23847142

  3. Hunter GR, Gower B, Kane B. Age related shift in visceral fat. Int J Body Comp Res 2010;8:103-8


    http://www.ncbi.nlm.nih.gov/pubmed/24834015

  4. Zhang G, Li J, Purkayastha S, et al. Hypothalamus programming of systemic ageing involving IKK-β, NF-κB and GnRH. Nature 2013;497:211-16


    http://www.ncbi.nlm.nih.gov/pubmed/23636330

  5. Lovejoy JC, Champagne CM, de Jonge L, Xie H, Smith SR. Increased visceral fat and decreased energy expenditure during the menopausal transition. Int J Obes 2008;32:949-58


    http://www.ncbi.nlm.nih.gov/pubmed/18332882

  6. Zivkovic TB, Vuksanovic M, Jelic MA, et al. Obesity and metabolic syndrome during the menopausal transition in Serbian women. Climacteric 2011;14:643-8


    http://www.ncbi.nlm.nih.gov/pubmed/21878054

  7. Lambrinoudaki I, Brincat M, Erel CT, et al. EMAS position statement: managing obese postmenopausal women. Maturitas 2010;66:323-6


    http://www.ncbi.nlm.nih.gov/pubmed/20434858