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Hyperemesis Gravidarum (HG) is a debilitating condition characterized by severe nausea and vomiting during pregnancy, yet its severity is often misunderstood or underestimated by both the public and healthcare providers. This lack of understanding can lead to misdiagnosis, inadequate treatment, and undue suffering for individuals experiencing HG. This study explores the online discourse surrounding HG to identify key themes related to patient experiences and perceptions. Using the Twint0 application, we collected 5,856 relevant posts from the X social networking site over a 12-month period. A thematic analysis revealed four major themes: (1) misconceptions about severity of symptoms, (2) emotional and psychological toll of HG, (3) experiences with healthcare and treatment, and (4) impact on pregnancy and maternal health. The findings highlight the urgent need for greater awareness and understanding of HG, particularly within healthcare settings, to improve diagnosis and treatment. Additionally, the study emphasizes the importance of patient-centered care and mental health support to address the emotional challenges faced by women with HG. [ABSTRACT FROM AUTHOR]

Clinically, SSRIs are widely prescribed in the treatment of several anxiety disorders, although very few pre-clinical studies have observed a beneficial effect of this class of drugs in animal models of anxiety. Furthermore, the biphasic pattern observed clinically, an exacerbation of anxiety followed by beneficial effects, is rarely observed in animal studies. In the present study we document this clinical phenomenon in several behavioural paradigms. While a single injection of citalopram induced anxiogenic effects, three administrations of citalopram were sufficient to elicit anxiolytic effects. Congruent with these data, we observed that short-term repeated administration of citalopram was accompanied by increased activation of cAMP response element-binding protein (CREB) in the hippocampus and desensitization of 5-HT1A receptors, two phenomena well associated with chronic rather than acute actions of antidepressants. Moreover, effects of citalopram were abolished in CREBαΔ mutant animals in the elevated zero maze (EZM) and tail suspension test (TST), but not in novelty-induced hypophagia (NIH). Further, the desensitization of 5-HT1A receptors elicited by citalopram was not affected by CREB deficiency. The significance of the EZM and TST paradigms in predicting therapeutic efficacy is well known while effects in NIH and 5-HT1A sensitization are less well-established. These data demonstrate that behavioural responses to citalopram are dependent on the frequency of its administration, and that these responses are differentially dependent on CREB function. [ABSTRACT FROM AUTHOR]

cAMP response element-binding protein (CREB) has been implicated in the molecular and cellular mechanisms of chronic antidepressant (AD) treatment, although its role in the behavioral response is unclear. CREB-deficient (CREBαΔ mutant) mice demonstrate an antidepressant phenotype in the tail suspension test (TST) and forced-swim test. Here, we show that, at baseline, CREBαΔ mutant mice exhibited increased hippocampal cell proliferation and neurogenesis compared with wild-type (WT) controls, effects similar to those observed in WT mice after chronic desipramine (DMI) administration. Neurogenesis was not further augmented by chronic DMI treatment in CREBαΔ mutant mice. Serotonin depletion decreased neurogenesis in CREBαΔ mutant mice to WT levels, which correlated with a reversal of the antidepressant phenotype in the TST. This effect was specific for the reversal of the antidepressant phenotype in these mice, because serotonin depletion did not alter a baseline anxiety-like behavior in CREBαΔ mutant mice. The response to chronic AD treatment in the novelty-induced hypophagia (NIH) test may rely on neurogenesis. Therefore, we used this paradigm to evaluate chronic AD treatment in CREBαΔ mutant mice to determine whether the increased neurogenesis in these mice alters their response in the NIH paradigm. Whereas both WT and CREBαΔ mutant mice responded to chronic AD treatment in the NIH paradigm, only CREBαΔ mutant mice responded to acute AD treatment. However, in the elevated zero maze, DMI did not reverse anxiety behavior in mutant mice. Together, these data show that increased hippocampal neurogenesis allows for an antidepressant phenotype as well as a rapid onset of behavioral responses to AD treatment. [ABSTRACT FROM AUTHOR]

Psychosocial stress, driven by a variety of sources and influences, can be ubiquitous in our modern society. Prolonged exposure to these stressors can have detrimental biological and psychological effects; extant findings in childhood adversity indicate that the cumulative effects of exposure to childhood adversity increase risk for developmental delays, altered immune responses, and psychopathology later in life. The pathways by which these effects are conferred continue to be studied. Given that pregnancy is a critical period during which susceptibility to lifetime health and illness are programmed, this chapter will focus on the impacts of maternal history of childhood adversity on offspring mental health, including the role of the microbiota-gut-brain axis. One of the most commonly used frameworks of the last several decades for measuring childhood adversity is the Adverse Childhood Experiences (ACEs) psychometric. We provide an overview of the possible mechanisms through which maternal stress, including the cumulative effects of maternal ACEs, may increase susceptibility to disease in offspring. These include altered epigenetic regulation, hypothalamic-pituitary-adrenal axis function and peripheral inflammation, and gut microbial composition. Finally, we conclude with clinical considerations, including possible future therapeutic interventions., (© 2021 S. Karger AG, Basel.)