Childhood Traumas in Obese Women: Association With Deregulation of the Glucocorticoid Axis and Inflammatory State.

We postulate that childhood traumas are associated with deregulation of the glucocorticoid axis and the inflammatory system in obese women. The main objective of the study is to compare the salivary cortisol awaking response in obese women according to the presence of childhood trauma (assessed using the Childhood Trauma Questionnaire, CTQ).

Obesity is an epidemic disease whose onset and development factors go beyond the simple energy balance. Current management strategies are often failing. It is therefore important to identify the underlying determinants of weight gain. The association of obesity in adulthood with trauma in childhood is now well established. However, the biological factors that account for this association are imperfectly known. The measurement of cortisol seems to be the most relevant biological marker of the link between obesity and life events. The majority of studies show that obesity is associated with increased exposure to glucocorticoids. However, some authors have recently reported that these measures are impacted by significant inter-individual variability which could be explained by differences in life events and especially in their perception. In addition, the autonomic nervous system with the secretion of catecholamines by the adrenal leads to the release of pro-inflammatory cytokines, resulting in a low grade inflammation.

The existence of childhood traumas and the association with other psychopathological disorders will be assessed using psychometric scales validated in French. The corticotropic axis will be evaluated by measuring cortisol in different matrices (saliva, urine, hair). The inflammatory state will be studied thanks to the determination of pro-inflammatory cytokines level in blood and immunophenotyping of myeloid-derived suppressor cells.

Eligibility Criteria:
Inclusion Criteria:

* ≥18 years female BMI≥30kg/m2

Exclusion Criteria:

1. History of bariatric surgery
2. Any condition or pathology that may influence the corticotropic axis or that may modify the excretion or dosage of cortisol:

   * pregnancy, breastfeeding
   * hepatocellular insufficiency,
   * severe heart failure,
   * mild/moderate acute heart failure,
   * any psychological disorder not stabilised for at least one year
   * alcohol or drug dependence, not weaned for at least one year
   * neoplasm under treatment
3. Current infectious disease or a history of autoimmune disease (except autoimmune hypothyroidism), inflammatory disease and/or neurodegenerative disease
4. Presence of an adrenal adenoma or any known or suspected clinical adrenal or corticotropic disorder
5. Subjects with a positive diagnosis of hypercorticism or suspected hypercorticism will also be excluded: 8-hour plasma cortisol after Dexamethasone suppression test (DST) (1 mg dexamethasone taken orally at midnight the previous day) greater than 1.8 microg/100 ml (50 nmol/l)
6. antidepressant and neuroleptic treatment, benzodiazepine treatment
7. treatment(s) likely to modify the exploration of the corticotropic axis: systemic or local corticosteroid therapy or glucocorticoid infiltration for less than 6 months
8. current use of anti-inflammatory drugs or antibiotics
9. Shift worker