Early Life Trauma, Emotion Dysregulation and Hormonal Sensitivity Across Female Reproductive Life Events.

PURPOSE OF REVIEW: To explore the relationship between early life trauma, hormonal sensitivity, and psychiatric disorders across female-reproductive life events, with a focus on the neurobiological mechanisms. RECENT FINDINGS: Childhood trauma significantly increases the risk of subsequent mood disorders during periods of intense hormonal fluctuation such as premenstrual, pregnancy, postpartum, and perimenopause. Neurobiological changes resulting from early trauma influence emotion regulation, which emerges as a key predisposing, exacerbating, and perpetuating factor to hormonal sensitivity and subsequent psychiatric symptoms. We identified altered stress response and allopregnanolone imbalance, bias in cognitive processing of emotions, neuroimage correlates and sleep disturbances as potential underlying neurobiological mechanisms. This review integrates cumulative findings supporting a theoretical framework linking early life trauma to hormonal sensitivity and mood disorders. We propose that some women might be more susceptible to such hormonal fluctuations because of emotion dysregulation following significant early life trauma.

Mood sensitivity to estradiol predicts depressive symptoms in the menopause transition.

BACKGROUND: The risk for depression markedly rises during the 5-6 years leading up to the cessation of menstruation, known as the menopause transition. Exposure to extreme estradiol levels may help explain this increase but few studies have examined individual sensitivity to estradiol in predicting perimenopausal depression. METHOD: The current study recruited 101 perimenopausal women. During Phase 1, we quantified each woman's sensitivity to changes in estradiol using 12 weekly measures of estrone-3-glucuronide (E1G), a urinary metabolite of estradiol, and concurrent depressive symptoms. The weekly cortisol awakening response was measured to examine the hypothalamic-pituitary-adrenal (HPA) axis in mediating mood sensitivity to estradiol. In Phase 2, depressive symptoms and major depression diagnoses were assessed monthly for 9 months. The relationship between Phase 1 E1G sensitivity and Phase 2 depressive symptoms and major depressive episodes was examined. Several baseline characteristics were examined as potential moderators of this relationship. RESULTS: The within-person correlation between weekly E1G and mood varied greatly from woman to woman, both in strength and direction. Phase 1 E1G mood sensitivity predicted the occurrence of clinically significant depressive symptoms in Phase 2 among certain subsets of women: those without a prior history of depression, reporting a low number of baseline stressful life events, and reporting fewer months since their last menstrual period. HPA axis sensitivity to estradiol fluctuation did not predict Phase 2 outcomes. CONCLUSION: Mood sensitivity to estradiol predicts risk for perimenopausal depression, particularly among women who are otherwise at low risk and among those who are early in the transition.

Delayed access to feed alters gene expression associated with hormonal signaling, cellular differentiation, and protein metabolism in muscle of newly hatch chicks.

Birds rely solely on utilization of the yolk sac as a means of nutritional support throughout embryogenesis and early post-hatch, before first feeding occurs. Newly hatched broiler (meat-type) chickens are frequently not given immediate access to feed, and this can result in numerous alterations to developmental processes, including those that occur in muscle. The objective of this study was to characterize the gene expression profile of newly hatched chicks' breast muscle with regards to hormonal regulation of growth and metabolism and development and differentiation of muscle tissue, and determine impacts of delayed access to feed on these profiles. Within 3 h of hatch, birds were placed in battery pens and given immediate access to feed (Fed) or delayed access to feed for 48 h (Delayed Fed). Breast muscle collected from male birds at hatch, or 4 h, 1 day (D), 2D, 4D, and 8D after hatch was used for analysis of mRNA expression by reverse transcription-quantitative PCR. Under fully fed conditions, insulin-like growth factor receptor and leptin receptor mRNA expression decreased as birds aged; however, delayed access to feed resulted in prolonged upregulation of these genes so their mRNA levels were higher in Delayed Fed birds at 2D. These expression profiles suggest that delayed feed access alters sensitivity to hormones that may regulate muscle development. Myogenin, a muscle differentiation factor, showed increasing mRNA expression in Fed birds through 2D, after which expression decreased. A similar expression pattern in Delayed Fed birds was deferred until 4D. Levels of myostatin, a negative regulator of muscle growth, increased in Fed birds starting at 2D, while levels in Delayed Fed birds began to increase at 4D. In Fed birds, levels of transcripts for two genes associated with protein catabolism, F-box protein 32 and forkhead box O3, were lower at 2D, while Delayed Fed mRNA levels did not decrease until 4D. Mechanistic target of rapamycin mRNA levels decreased from 1D through 8D in both treatments, except for a transient increase in the Delayed Fed birds between 1D and 2D. These data suggest that within breast muscle, delayed feeding alters hormonal signaling, interrupts tissue differentiation, postpones onset of growth, and may lead to increased protein catabolism. Together, these processes could ultimately contribute to a reduction in proper growth and development of birds not given feed immediately after hatch, and ultimately hinder the long-term potential of muscle accretion in meat type birds.

The hormonal sensitivity hypothesis: A review and new findings.

Previous women's health practitioners and researchers have postulated that some women are particularly sensitive to hormonal changes occurring during reproductive events. We hypothesize that some women are particularly sensitive to hormonal changes occurring across their reproductive lifespan. To evaluate this hypothesis, we reviewed findings from the existing literature and findings from our own lab. Taken together, the evidence we present shows a recurring pattern of hormonal sensitivity at predictable but different times across the lifespan of some women (i.e., menarche, the premenstrual phase, hormonal contraceptive use, pregnancy, the postpartum period, and menopause). These findings provide support for the hypothesis that there is a subgroup of women who are more susceptible to physical, psychological, and sexual symptoms related to hormonal shifts or abrupt hormonal fluctuations that occur throughout the reproductive lifespan. We propose that this pattern reflects a Hormonal Sensitivity Syndrome.