Leptin levels are associated with decreased depressive symptoms in women across the weight spectrum, independent of body fat

Harvard University, Cambridge, Massachusetts, United States
Clinical Endocrinology (Impact Factor: 3.46). 07/2011; 76(4):520-5. DOI: 10.1111/j.1365-2265.2011.04182.x
Source: PubMed


Leptin is anorexigenic, and levels are markedly decreased in women with low body weight and high in women with obesity. Ghrelin opposes leptin effects on appetite and is negatively associated with body mass index. These appetite-regulating hormones may have opposing effects on mood and stress pathways. Women with anorexia nervosa (AN), hypothalamic amenorrhoea (HA) and obesity are at increased risk of depression and anxiety. It is unknown whether dysregulation of leptin or ghrelin contributes to the development of depression and/or anxiety in these disorders. We investigated the relationship between leptin and ghrelin levels and symptoms of depression, anxiety and perceived stress in women across the weight spectrum.
64 women: 15 with AN, 12 normal-weight with HA, 17 overweight or obese (OB) and 20 normal-weight in good health (HC).
Fasting serum leptin and plasma ghrelin levels were measured. Hamilton Rating Scales for Depression (HAM-D) and Anxiety (HAM-A) and the Perceived Stress Scale were administered.
Leptin levels were inversely associated with HAM-D, HAM-A and Perceived Stress scores. The negative relationships between leptin and severity of symptoms of both depression and anxiety remained significant after controlling for body fat or weight. There was no relationship between ghrelin and symptoms of depression or anxiety. Although ghrelin levels were positively associated with the degree of perceived stress, this relationship was not significant after controlling for body fat or weight.
Leptin may mediate depressive symptoms across the weight spectrum. Further investigation of the role of leptin in modulating mood will be important.

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    • "By contrast, leptin-deficient (ob/ob) mice exhibit increased anxiety behaviors in multiple behavioral tests (Asakawa et al., 2003;Finger et al., 2010). Moreover, clinical research reported that plasma leptin levels are correlated with anxiety states (Lawson et al., 2012;Yoshida-Komiya et al., 2014). These studies support an important role for leptin in the regulation of anxiety-related behaviors. "

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    • "Defining and characterizing this putative subgroup may help to advance our understanding of the association between depression and poor fetal growth. In addition to these findings with depression, lower serum leptin levels in women have been associated with anxiety symptoms and perceived stress [26]. Disrupted leptin signaling is also implicated in poor fetal growth as evidence suggests that growth impaired pregnancies are characterized by altered leptin physiology in cord blood293031, placenta [32, 33], and maternal serum [34], although reports on maternal serum have varied in designs and results34353637383940414243). "
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    ABSTRACT: We sought to identify and characterize predictors of poor fetal growth among variables extracted from perinatal medical records to gain insight into potential etiologic mechanisms. In this process we reevaluated a previously observed association between poor fetal growth and maternal psychiatric disease. We evaluated 449 deliveries of >36 weeks gestation that occurred between 9/2008 and 9/2010 at the Women and Infants Hospital in Providence Rhode Island. This study group was oversampled for Small-for-Gestational-Age (SGA) infants and excluded Large-for-Gestational-Age (LGA) infants. We assessed the associations between recorded clinical variables and impaired fetal growth: SGA or Intrauterine Growth Restriction (IUGR) diagnosis. After validating the previously observed association between maternal psychiatric disease and impaired fetal growth we addressed weaknesses in the prior studies by explicitly considering antidepressant use and the timing of symptoms with respect to pregnancy. We then evaluated DNA methylation levels at 27 candidate loci in placenta from a subset of these deliveries (n = 197) to examine if epigenetic variation could provide insight into the mechanisms that cause this co-morbidity. Infants of mothers with prenatal psychiatric disease (Depression, Anxiety, OCD/Panic) had increased odds of poor fetal growth (ORadjusted = 3.36, 95%CI: 1.38-8.14). This relationship was similar among those who were treated with antidepressants (ORadjusted = 3.69, 95%CI: 1.31-10.45) and among those who were not (ORadjusted = 3.19, 95%CI: 1.30-7.83). Among those with a history of psychiatric disease but no active disease in pregnancy the ORadjusted was 0.45 (95%CI: 0.09-2.35). A locus near the transcription start site of the leptin receptor (cg21655790) had methylation levels that were decreased in the presence of: 1) SGA/IUGR, and 2) active but not resolved psychiatric disease (among mothers not on antidepressants). These results validate and further characterize the association between maternal psychiatric disease and poor fetal growth. Because the association appears to depend on active psychiatric disease, this suggests a transient and potentially modifiable pathophysiology. The molecular findings in this study suggest that altered leptin signaling may be involved in the biological mechanisms that link prenatal maternal psychiatric symptoms and poor fetal growth.
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    • "Therefore, chronodisruption in appetite hormones may provoke a disregulation in the aminergic pathway and vice versa. A study that investigated the relationship between leptin levels and ghrelin as well as symptoms of depression, anxiety and stress in women demonstrated a significantly negative relationship between leptin and the severity of depressive symptoms and anxiety (Lawson et al., 2012). Females present a greater expression of clock genes in adipose tissue, and consequently, it has been hypothesized that this sexual dimorphism may account for the different CT of males and female (Gómez-Abellán et al., 2012). "

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