Middle age has been linked with various dysfunctional eating patterns in women. The hormone ghrelin is related to food intake, with plasma levels rising before eating and decreasing immediately afterwards. Animal research has shown that oestradiol is an antagonist of ghrelin. Given that both menopause and anorexia nervosa (AN) are states characterised by reduced oestradiol, the present study aimed to investigate for the first time whether menopausal status and a history of AN are linked with altered ghrelin levels in middle‐aged women. Based on previous research, we hypothesised that (i) post‐menopausal women would demonstrate comparably increased ghrelin after food intake and (ii) women with a history of AN would exhibit increased total ghrelin levels. Healthy, middle‐aged women (n = 57) were recruited. Of the women, 31 were post‐menopausal and 27 had a history of AN. Plasma ghrelin was repeatedly collected before and after a meal standardised in terms of caloric content. Areas under the curves were calculated to indicate total (AUCg) and postprandial ghrelin (AUCi). Menopausal status was linked with postprandial ghrelin (AUCi −1.6 ± 2.2 vs −2.9 ± 2.6; P = 0.058), whereas a history of AN was linked with total ghrelin (AUCg 36.2 ± 5.6 vs 39.0 ± 3.7; P = 0.050). There were no interaction effects (both P > 0.466). A closer examination of the effects revealed that post‐menopausal women showed marginally greater decreases in ghrelin immediately after food intake (P = 0.064) and marginally greater re‐increases after 60 minutes (P = 0.084) compared to pre‐menopausal women. Women with a history of AN had significantly higher total ghrelin compared to women without a history of AN (P = 0.042). Post‐menopause was linked with higher sensitivity of ghrelin to food intake (trend), whereas a history of AN was related to greater total ghrelin. Future research should investigate to what extent the observed alterations in ghrelin may affect dysfunctional eating behaviour during middle age.

BACKGROUND: Weight gain is common as women approach mid-life. Reduced levels of leptin, an anorexigenic hormone, may facilitate this. Studies in middle-aged women with obesity have shown that dysfunctional eating behaviour, such as restrained eating, is linked to lower leptin. Furthermore, states of low oestradiol signalling, as are found in post-menopause or anorexia nervosa, have been found to impact leptin levels. The aim of this study was to investigate, for the first time, how different aspects of dysfunctional eating, menopausal status, and a history of anorexia nervosa relate to leptin levels in normalweight middle-aged women. METHODS: A total of N = 57 women were recruited. Thirty-one were postmenopausal, and 27 had a history of anorexia nervosa. Dysfunctional eating behaviour was measured by the Three-Factor Eating Questionnaire, which contains three subscales: susceptibility/responsiveness to hunger, restraint, and disinhibition. Body composition was assessed by bioelectrical impedance analysis. A fasting blood sample was obtained to determine leptin. RESULTS: Controlling for age, body mass index, and fat mass, susceptibility/responsiveness to hunger was positively associated with leptin ( = 0.267, p = 0.031), whereas restrained eating ( = -0.183, p = 0.079) and a history of anorexia nervosa ( = -0.221, p = 0.059) were, by trend, negatively associated with leptin. Neither disinhibited eating nor menopausal status was related to leptin. CONCLUSIONS: Leptin may decline as a response to repeated states of a negative energy balance. A possible implication is that mid-life weight management should avoid extreme changes in eating behaviour and instead focus on the macronutrient composition of diet and physical activity. Further, longitudinal enquiries are warranted to investigate these relationships.