Cortisol in relation to problematic eating behaviours, adiposity and symptom profiles in Major Depressive Disorder.

Aims: Major Depressive Disorder (MDD) is associated with an increased risk of chronic disease related to weight gain, problematic eating behaviours and neuroendocrine changes. MDD is frequently associated with altered hypothalamic-pituitary-adrenal axis activity and cortisol secretion, where cortisol has been implicated in regulating energy balance, food intake and depressogenic weight changes. However, little research has examined the relationships between cortisol, adiposity and depressogenic problematic eating behaviours. Method: Plasma cortisol concentrations were compared between 37 participants with MDD reporting appetite/weight loss, 43 participants with MDD reporting appetite/weight gain, and 60 healthy controls, by sex. Associations between cortisol, indices of adiposity and problematic eating behaviours were then assessed after accounting for demographic variables and depressive symptoms. Depressive symptoms were assessed using the Depression subscale of the Depression, Anxiety and Stress Scale, and eating behaviours with the Dutch Eating Behaviours Questionnaire and Yale Food Addiction Scale. Results: Participants with MDD reporting appetite/weight loss had higher cortisol compared to controls, and marginally higher cortisol than those with MDD reporting appetite/weight gain. Cortisol negatively and significantly accounted for unique variance in body mass index and waist circumference after accounting for variance associated with age, sex and depressive symptoms, however it was not a significant predictor of problematic eating behaviours, such as emotional eating or food addiction. Cortisol concentrations did not differ between sexes. Conclusion: The results indicate that cortisol is related to lower indices of adiposity and depressogenic symptoms of appetite/weight loss but is not related to problematic eating behaviours and appetite increases in MDD. These findings provide further evidence that the melancholic and atypical subtypes of MDD are associated with differential neuroendocrine and anthropometric indices, as well as behavioural and symptom profiles. Further research investigating the temporal nature of the identified relationships may assist in facilitating the development of improved interventions for individuals affected by weight changes in MDD.

Overeating and food addiction in Major Depressive Disorder: Links to peripheral dopamine.

The concept of food addiction refers to addiction-like behaviours that develop in association with the intake of highly palatable foods. Previous research indicates that a high proportion of individuals with Major Depressive Disorder (MDD) meet the criteria for food addiction, and are also at an increased risk of weight gain and chronic disease. In the central nervous system, dopamine is a neurotransmitter associated with reward salience and food intake, whereas peripheral dopamine is involved in sympathetic stress regulation, digestion and gastrointestinal motility. However, little research has examined relationships between peripheral dopamine, depressive symptoms and problematic eating behaviours in MDD. Biometrics, psychopathology and plasma dopamine levels were compared between participants with MDD (n = 80) and controls (n = 60). Participants were sub-categorised into those meeting or not meeting Yale Food Addiction Scale (YFAS) criteria. Psychometric measures of mood and appetite were used to assess MDD symptoms, problematic eating behaviours and food-addiction related symptoms. Twenty-three (23; 29%) MDD participants met the Yale criteria for food addiction. Depressed individuals meeting YFAS criteria had significantly greater psychopathology scores for both mood and eating compared to depressed individuals not meeting YFAS criteria and controls. A significant interaction between food addiction status and sex was also observed for plasma dopamine levels. Plasma dopamine levels correlated positively with disordered eating behaviours in females, and negatively in males. The results provide evidence that depressogenic excess eating and weight gain are associated with peripheral dopamine levels. Longitudinal research is warranted investigating endocrine dysregulation and excess eating in MDD, which may inform interventions and reduce chronic disease risk in affected individuals.

Weight gain in Major Depressive Disorder: Linking appetite and disordered eating to leptin and ghrelin.

Major Depressive Disorder (MDD) involves changes in appetite and weight, with a subset of individuals at an increased risk of weight gain. Pathways to weight gain may include appetite disturbances, excess eating, and dysregulation of appetite hormones. However, little research has simultaneously examined relationships between hormones, eating behaviours and MDD symptoms. Plasma ghrelin and leptin, biometrics, eating behaviours and psychopathology were compared between depressed (n = 60) and control (n = 60) participants. Depressed participants were subcategorised into those with increased or decreased appetite/weight for comparison by subtype. The Dutch Eating Behaviours Questionnaire and Yale Food Addiction Scale measured eating behaviours. Disordered eating was higher in MDD than controls, in females than males, and in depressed individuals with increased, compared to decreased, appetite/weight. Leptin levels were higher in females only. Leptin levels correlated positively, and ghrelin negatively, with disordered eating. The results provide further evidence for high levels of disordered eating in MDD, particularly in females. The correlations suggest that excessive eating in MDD is significantly linked to appetite hormones, indicating that it involves physiological, rather than purely psychological, factors. Further, longitudinal, research is needed to better understand whether hormonal factors play a causal role in excessive eating in MDD.

Problematic eating behaviours, changes in appetite, and weight gain in Major Depressive Disorder: The role of leptin.

BACKGROUND: Appetite and weight changes are core symptoms of Major Depressive Disorder (MDD), and those with MDD are at increased risk of obesity, cardiovascular disease and metabolic disorders. Leptin promotes satiety, with leptin dysregulation and resistance noted in obesity. However, the role of leptin in weight changes in MDD is not established. This study investigates leptin levels in relation to appetite and weight changes and problematic eating behaviours in MDD. METHODS: Plasma leptin levels, psychopathology and biometrics were compared between participants meeting DSM-5 diagnostic criteria for MDD (n = 63) and healthy controls (n = 60). Depressed participants were also sub-categorised according to increased, decreased or unchanged appetite and weight. The Dutch Eating Behaviour Questionnaire and Yale Food Addiction Scale were examined in a subset of participants with MDD. RESULTS: Females with increased appetite/weight had higher leptin levels than those with stable or reduced appetite/weight, however males showed the opposite effect. Leptin levels were positively correlated with problematic eating behaviours. One quarter of the depressed subset, all females, met the Yale criteria for food addiction, approximately double the rates reported in general community samples. LIMITATIONS: The study is limited by a cross sectional design and a small sample size in the subset analysis of eating behaviours. CONCLUSIONS: The results provide new information about associations between leptin, sex-specific weight and appetite changes and problematic eating behaviours, which may be risk factors for cardiovascular and metabolic diseases in MDD, particularly in females. Future longitudinal research investigating leptin as a risk factor for weight gain in MDD is warranted, and may lead to early interventions aimed at preventing weight gain in at-risk individuals.