Prenatal Depressive Symptoms, Self-Rated Health, and Diabetes Self-Efficacy: A Moderated Mediation Analysis.

BACKGROUND: Diabetes leads to risk for pregnant persons and their fetuses and requires behavioral changes that can be compromised by poor mental health. Poor self-rated health (SRH), a reliable predictor of morbidity and mortality, has been associated with depressive symptoms and lower self-efficacy in patients with diabetes. However, it is unclear whether SRH mediates the association between depressive symptoms and self-efficacy in pregnant patients with diabetes and whether the healthcare site moderates the mediation. Thus, we sought to test these associations in a racially and ethnically diverse sample of pregnant individuals diagnosed with diabetes from two clinical settings. MATERIALS AND METHODS: This was an observational, cross-sectional study of 137 pregnant individuals diagnosed with diabetes at two clinical study sites. Participants self-administered a demographic questionnaire and measures designed to assess depressive symptoms, SRH in pregnancy, and diabetes self-efficacy. A moderated mediation model tested whether these indirect effects were moderated by the site. RESULTS: The results show that SRH mediated the association between depressive symptoms and diabetes self-efficacy. The results also showed the site moderated the mediating effect of SRH on depressive symptoms and diabetes self-efficacy. CONCLUSIONS: Understanding the role of clinical care settings can help inform when and how SRH mediates that association between prenatal depressive symptoms and self-efficacy in diabetic patients.

Association of microbial dynamics with urinary estrogens and estrogen metabolites in patients with endometriosis.

Endometriosis is an estrogen dependent gynecological disease associated with altered microbial phenotypes. The association among endogenous estrogen, estrogen metabolites, and microbial dynamics on disease pathogenesis has not been fully investigated. Here, we identified estrogen metabolites as well as microbial phenotypes in non-diseased patients (n = 9) and those with pathologically confirmed endometriosis (P-EOSIS, n = 20), on day of surgery (DOS) and ~1-3 weeks post-surgical intervention (PSI). Then, we examined the effects of surgical intervention with or without hormonal therapy (OCPs) on estrogen and microbial profiles of both study groups. For estrogen metabolism analysis, liquid chromatography/tandem mass spectrometry was used to quantify urinary estrogens. The microbiome data assessment was performed with Next generation sequencing to V4 region of 16S rRNA. Surgical intervention and hormonal therapy altered gastrointestinal (GI), urogenital (UG) microbiomes, urinary estrogen and estrogen metabolite levels in P-EOSIS. At DOS, 17ß-estradiol was enhanced in P-EOSIS treated with OCPs. At PSI, 16-keto-17ß-estradiol was increased in P-EOSIS not receiving OCPs while 2-hydroxyestradiol and 2-hydroxyestrone were decreased in P-EOSIS receiving OCPs. GI bacterial α-diversity was greater for controls and P-EOSIS that did not receive OCPs. P-EOSIS not utilizing OCPs exhibited a decrease in UG bacterial α-diversity and differences in dominant taxa, while P-EOSIS utilizing OCPs had an increase in UG bacterial α-diversity. P-EOSIS had a strong positive correlation between the GI/UG bacteria species and the concentrations of urinary estrogen and its metabolites. These results indicate an association between microbial dysbiosis and altered urinary estrogens in P-EOSIS, which may impact disease progression.

Alteration of systemic and uterine endometrial immune populations in patients with endometriosis.

PROBLEM: Endometriosis is defined as growth of endometrial tissue in ectopic locations; it is associated with infertility and chronic pain and affects ~12% of reproductive-aged women. Although inflammation is known to play a key role in endometriosis, knowledge related to immune phenotypes associated with this disease is lacking. This study aimed to characterize immune profiles in patients with endometriosis, to assess inflammatory mediators, to and determine if surgical and/or hormonal therapies restore immune homeostasis. METHODS OF STUDY: Samples from nine controls and 20 histologically confirmed endometriosis patients were collected upon surgery and ~1-3 weeks post-surgical intervention. Subjects were either not utilizing hormonal suppression or were currently on monophasic hormonal therapy. Tolerant regulatory T cells (Tregs = natural [nTregs] +inducible [iTregs]) and inflammatory T helper 17 (Th17) cells were identified in peripheral blood via flow cytometry and within the eutopic/ectopic endometrial tissues via immunohistochemistry and real-time-qPCR. Cytokines were assessed via 10-plex-ELISA. RESULTS: Patients with endometriosis not utilizing hormonal therapy exhibited lower iTregs (tolerant), greater Th17 (inflammatory), and a reduction in Treg/Th17 ratio (P < .05), indicative of systemic inflammation. Treg and Th17 localizations were enhanced within the ectopic endometrial implant, which promotes lesion development. Hormonal therapy decreased systemic and local inflammation (eutopic/ectopic endometrium) via decreased iTregs and Th17 cells in patients with endometriosis (P < .05). Thus, imbalance within immune populations correlated with increased inflammation in patients with endometriosis, which was mitigated by hormonal therapy. CONCLUSIONS: Patients with endometriosis exhibited systemic and localized inflammation within ectopic and endometrial tissues. Hormonal therapy dampened inflammation caused by disease.

An association of intrapartum synthetic oxytocin dosing and the odds of developing autism.

LAY ABSTRACT: Oxytocin is a hormone naturally produced in the human body that can make the womb (uterus) contract during labor. Manufactured oxytocin is frequently given to mothers in labor to strengthen the contractions or in some cases to start labor. This study compared children with a diagnosis of autism and children without autism to see whether children with autism received more oxytocin during labor. The odds of a child having an autism diagnosis were significantly higher if the delivery was a first-time Cesarean section, if the mother had a body mass index of 35 or higher, or if the reason for delivery were a range of fetal problems that made delivery necessary. It was found that boys who were exposed to oxytocin for longer periods of time during labor and received higher total doses of oxytocin had significantly higher odds of developing autism. There were no significant associations of oxytocin dosing and autism noted in female children. As this is the first study to look at any relationship between the dose of oxytocin received during labor and the odds of developing autism, further study needs to be done to determine whether there is any cause and effect relationship. Thus, at this time, there is no recommended change in clinical practice.