Non-Pharmacologic Interventions for Hemodynamic Stability During Dental Implant Surgery: A Randomized Controlled Trial.

Uterine fibroids, or uterine leiomyomas, are the most common benign tumors in women, with around 200,000 cases reported annually. Black women are disproportionately affected, with approximately 80% developing fibroids at some point in their lives compared to 70% of Caucasian women. Fibroids are hormone-dependent tumors, primarily thriving on estrogen, which means they often develop after the onset of menstruation and typically shrink after menopause []. The primary symptoms of fibroids include heavy, prolonged, and/or irregular menstrual bleeding, pelvic pain, frequent urination, constipation, and pain during intercourse, all of which can significantly impact a woman’s quality of life. The reasons for the higher incidence of fibroids among Black women are not fully understood but several factors have been proposed. Growing evidence suggests that chronic psychosocial stress from environmental exposures, in conjunction with genetic susceptibility, may be associated with the development or worsening of uterine fibroids, though direct causal relationships remain incompletely established. The physical symptoms associated with uterine fibroids are frequently accompanied by psychological distress, including depression and anxiety disorders [], suggesting a potentially bidirectional relationship in which stress may contribute to fibroid pathology while fibroid burden may, in turn, exacerbate psychological stress. Allostatic load refers to the cumulative physiological and psychological burden that accrues when the body’s stress-response systems are repeatedly or chronically activated beyond their adaptive capacity. Under normal conditions, the body maintains internal stability through homeostatic mechanisms, mounting a coordinated stress response—mediated primarily by the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system—that resolves once the stressor has passed. However, when stressors are prolonged, repeated, or perceived as uncontrollable, these same adaptive systems can become dysregulated, shifting from protective to pathological. Individual susceptibility to this transition is shaped by genetic predisposition, early life experiences, and environmental context, which collectively modulate both the magnitude and duration of the stress response []. The biological consequences of sustained allostatic load are multisystemic. At the neuroendocrine level, chronic stress activates the pituitary gland to release adrenocorticotropic hormone (ACTH), which in turn drives adrenal secretion of cortisol. While cortisol is essential for short-term metabolic and immune regulation, its chronic elevation disrupts the negative feedback mechanisms that normally constrain HPA axis activity. This dysregulation has been associated with a broad range of adverse health outcomes, including hypertension, type 2 diabetes, musculoskeletal disorders, periodontal disease, reproductive dysfunction, and malignancy. Chronically elevated cortisol also promotes oxidative stress—defined as an imbalance between reactive oxygen species (ROS) production and antioxidants—with downstream consequences including DNA and RNA damage [].