The late-luteal leptin level, caloric intake and eating behaviors among women with premenstrual dysphoric disorder
Introduction
Premenstrual dysphoric disorder (PMDD) was included as an official diagnostic criteria in the DSM 5 in 2012 (American Psychiatric Association, 2012) based on adequate evidence (Epperson et al., 2012). It is defined as having predictable, cyclic, and functional-impairing psychological and somatic symptoms, such as depression, irritability, lethargy or hypersomnia. These symptoms are aggravated in the late-luteal phase of the menstrual cycle and resolved by menstruation (Rapkin and Winer, 2009). Marked changes in appetite and overeating are typical concomitant PMDD symptoms (American Psychiatric Association, 2012) and are affected by the menstrual cycle among women with PMDD (Yen et al., 2010). Evaluation of hormones that fluctuate during the menstrual cycle and affect eating behavior, such as leptin, may provide insight into the mechanism of overeating symptoms among women with PMDD.
Food intake is reduced in the periovulatory phase and increased during the luteal phase among women (Buffenstein et al., 1995, Dye and Blundell, 1997, Van Vugt, 2010), particularly among those with PMDD (Evans et al., 1999, McNeil and Doucet, 2012). Women with PMDD have been reported to eat more calories in the late-luteal phase than in the follicular phase as compared with control women (Reed et al., 2008). Further, sweet food craving is exacerbated in the late-luteal phase among women with PMDD (Yen et al., 2010). These results indicated that women with PMDD increase their food intake in the late-luteal phase. However, whether women with PMDD have an increased caloric intake and an increased sweet caloric intake in the late-luteal phase as compared with healthy women has not been empirically evaluated throughout the menstrual cycle. Additionally, the underlying factors contributing to the changes in caloric intake among women with PMDD are not well-understood (McNeil and Doucet, 2012).
Leptin, a hormone secreted by adipocytes, acts on the hypothalamus to regulate appetite and neuroendocrine function (Cohen, 2006). Leptin has a role in ovulation through its stimulation of the pituitary to secrete luteinizing hormone (LH) (Fenichel et al., 2008). The administration of recombinant leptin has been shown to restore menses and fertility in women with hypothalamic or leptin deficiency amenorrhea (Chou et al., 2011, von Schnurbein et al., 2012). Recent studies have demonstrated that the leptin level is increased over the menstrual cycle, with a mid-cycle peak concurrent with the LH surge (Ahrens et al., 2014). These studies all indicated that leptin is related to not only eating behavior, but also to the menstrual cycle (Goumenou et al., 2003). One study revealed a significant decline in leptin among women with PMDD in comparison with controls (Akturk et al., 2013). As leptin plays key roles in the menstrual cycle and appetite and has been found to be altered among women with PMDD, further study is necessary to evaluate the alterations in the leptin level and their effects on the caloric intake of women with PMDD (Akturk et al., 2013).
Further, leptin is transported across the blood-brain-barrier by a saturable transporter system and exerts its anorectic effect via the hypothalamic arcuate nucleus. It results in a reduced food intake and an increased energy expenditure (Suzuki et al., 2012). However, obese individuals often have high leptin levels, which result in a failure to respond to exogenous leptin (Suzuki et al., 2012). Obesity has been reported to be associated with PMDD (Masho et al., 2005). The moderating effect of being overweight should be considered when evaluating the association between leptin and caloric intake. Further, there exist complex associations between the menstrual cycle, leptin level, eating behavior, obesity, and PMDD (McNeil and Doucet, 2012), and evaluation of these factors across the menstrual cycle with analysis separately in overweight and normal-weight women may provide insight into the effect of leptin on the late-luteal caloric intake among women with PMDD.
Aside from hormone levels, mood, stress, and rewarding characteristics contribute to overeating behavior (Jauch-Chara and Oltmanns, 2014). Depression and irritability are the cardinal symptoms of PMDD (Ko et al., 2013, Yen et al., 2011). Emotional eating is an eating behavior motivated by multiple negative emotions (Chesler, 2012) and moderate stress-induced food intake in females (van Strien et al., 2014). Further, women with PMDD have a higher impulsivity (Yen et al., 2011). Impulsivity is associated with uncontrolled eating (Leitch et al., 2013), a tendency to eat more than usual due to a loss of control over intake (Karlsson et al., 2000), and contributes to caloric intake (Kronick et al., 2011). Women with PMDD also have impaired inhibitory control (Yen et al., 2013). The inhibitory control function is associated with cognitive restraint, conscious restriction of food intake in order to control body weight or to promote weight loss (Leitch et al., 2013). Cognitive restraint has been reported to associate with caloric intake among women with PMDD (Evans et al., 1999). Thus, whether three factors related to eating behavior, including cognitive restraint, uncontrolled eating and emotional eating, contribute to caloric intake should be evaluated among women with PMDD.
Thus, the aims of the study were to evaluate: (1) whether the menstrual cycle (late-luteal phase versus follicular phase) or PMDD (PMDD group versus controls) have impacts on the leptin level, caloric intake, and eating behaviors; (2) whether being overweight moderates the association between leptin level and caloric intake; (3) the differences in leptin level, caloric intake and eating behaviors between women with PMDD and controls among overweight and normal-weight subjects; (4) whether eating behaviors are associated with late-luteal caloric intake among normal-weight or overweight women with PMDD.
Section snippets
Participants
Subjects were recruited using an advertisement posted specifically to attract a PMDD group without treatment and a control group on a university campus from 08/2011 to 10/2012. Volunteers in the PMDD group had a positive response to five or more premenstrual symptoms of the eleven DSM-IV-TR criteria of PMDD (American Psychiatric Association, 2000). The control group had positive responses to fewer than 2 of those criteria or had no functional impairment under mild symptoms. Subjects currently
Results
According to the definition of a symptomatic cycle in PMDD, women with PMDD should have a PMDDSQ score in the late-luteal phase that is 30% higher than the individual minimal score in the menstrual cycle (Smith et al., 2003). Further, the score on the PMDDSQ in the late-luteal phase among women with PMDD should be higher than the mean plus two standard deviations of that in the control group. A total of 16 PMDD candidates were excluded from the PMDD group because they did not meet the criteria
The eating behaviors of the women with PMDD
The severity of PMDD symptoms was found to be associated with increased late-luteal caloric intake (Giannini et al., 1985). In line with a previous report (Reed et al., 2008), the women with PMDD exhibited a greater increase in caloric intake in the late-luteal phase than the controls. This might contribute to a greater body weight (Yen et al., 2010) or a higher cholesterol level (Hsiao et al., 2011). Further, uncontrolled eating was exacerbated significantly in the late-luteal phase among the
Role of the funding source
Funding for this study was provided by National Science Council and the Kaohsiung Medical University Hospital; the National Science Council and the Kaohsiung Medical University Hospital had no further role in study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication.
Conflict of interest
The authors declare no conflict of interest.
Acknowledgments
This study was supported by grants from the National Science Council Taiwan (NSC 100-2629-B-037-001-MY2) and the Kaohsiung Medical University Hospital (KMUH100-0R51).
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