scholarly journals 827Early life influences on timing of menarche in racial/ethnic minority and immigrant women

2021 ◽  
Vol 50 (Supplement_1) ◽  
Author(s):  
Ayana April-Sanders ◽  
Parisa Tehranifar ◽  
Erica Lee Argov ◽  
Shakira Suglia ◽  
Jasmine McDonald
Keyword(s):  
Ethnic Minority ◽  
Mentally Ill ◽  
Early Life ◽  
Childhood Adversity ◽  
Reproductive Development ◽  
Age At Menarche ◽  
Early Life Adversity ◽  
Early Menarche ◽  
History Of ◽  
Racial Ethnic

Abstract Background Early life adversity and infections may theoretically affect the timing and effort of reproductive development. We examined associations of childhood adversity and exposure to tonsillitis with age at menarche in women age 40-64 years. Methods A multi-ethnic cohort of 394 women reported on exposure to parental maltreatment and maladjustment during childhood (<18 years) and on any diagnosis of tonsillitis, an infection primarily acquired in early life and adolescence. We used linear and logistic regression models to examine the associations of cumulative/specific childhood adversity experience(s) and history of tonsillitis with average age at menarche and early onset of menarche (<12 years of age). Results The average age at menarche was 12.6 years, and was significantly lower for women who lived with a mentally ill caregiver (M = 12.4 (95% CI: 11.7-13.0)) and those with a history of tonsillitis (M = 12.6 (95% CI: 12.0-13.2)). In adjusted multivariable models, living with a mentally ill caretaker (RR = 1.5, 95% CI: 1.0-2.1) and a having a history of tonsillitis (RR = 1.7, 95% CI: 1.3-2.4) were associated with increased risk of early menarche compared with women without these exposures. Cumulative and other specific adversities were not statistically associated with early menarche. Conclusions These findings support growing evidence that early life experiences may influence reproductive development. Key messages Early life adversity related to living with mentally ill caretakers and a history of tonsillitis is associated with earlier menarche in racial/ethnic minority and immigrant women.

scholarly journals Influence of Childhood Adversity and Infection on Timing of Menarche in a Multiethnic Sample of Women

2021 ◽  
Vol 18 (8) ◽  
pp. 4080
Author(s):  
Ayana K. April-Sanders ◽  
Parisa Tehranifar ◽  
Erica Lee Argov ◽  
Shakira F. Suglia ◽  
Carmen B. Rodriguez ◽  
...  
Keyword(s):  
Early Life ◽  
Life Experiences ◽  
Childhood Adversity ◽  
Reproductive Development ◽  
Age At Menarche ◽  
Multiethnic Cohort ◽  
History Of ◽  
Timing Of Menarche ◽  
Parental Maltreatment ◽  
Multiethnic Sample

Childhood adversities (CAs) and infections may affect the timing of reproductive development. We examined the associations of indicators of CAs and exposure to tonsillitis and infectious mononucleosis (mono) with age at menarche. A multiethnic cohort of 400 women (ages 40–64 years) reported exposure to parental maltreatment and maladjustment during childhood and any diagnosis of tonsillitis and/or mono; infections primarily acquired in early life and adolescence, respectively. We used linear and relative risk regression models to examine the associations of indicators of CAs individually and cumulatively, and history of tonsillitis/mono with an average age at menarche and early onset of menarche (<12 years of age). In multivariable models, histories of mental illness in the household (RR = 1.44, 95% CI: 1.01–2.06), and tonsillitis diagnosis (RR = 1.67, 95% CI: 1.20–2.33) were associated with early menarche (<12 years), and with an earlier average age at menarche by 7.1 months (95% CI: −1.15, −0.02) and 8.8 months (95% CI: −1.26, −0.20), respectively. Other adversities indicators, cumulative adversities, and mono were not statistically associated with menarcheal timing. These findings provided some support for the growing evidence that early life experiences may influence the reproductive development in girls.

Childhood trajectories of anxiousness and disruptiveness explain the association between early-life adversity and attempted suicide

2012 ◽  
Vol 42 (11) ◽  
pp. 2373-2382 ◽  
Author(s):  
B. Wanner ◽  
F. Vitaro ◽  
R. E. Tremblay ◽  
G. Turecki
Keyword(s):  
Mental Disorders ◽  
Suicidal Behavior ◽  
Early Life ◽  
Suicide Attempts ◽  
Childhood Adversity ◽  
Externalizing Disorders ◽  
Mediating Effect ◽  
Early Life Adversity ◽  
History Of ◽  
Axis I

BackgroundSuicidal behavior is frequently associated with a history of childhood abuse yet it remains unclear precisely how early life adversity may increase suicide risk later in life. As such, our aim was to examine whether lifetime trajectories of disruptiveness and anxiousness trait dysregulation explain the association between childhood adversity and suicidal behavior; and moreover, to test the potential modifying effects of mental disorders on these associations.MethodA sample of 1776 individuals from a prospective school-based cohort followed longitudinally for over 22 years was investigated. We tested the influence of disruptiveness and anxiousness trajectories from age 6 to 12 years on the association between childhood adversity (i.e. sexual and physical abuse) and history of suicide attempts (SA) using logistic regression models. Both adolescent externalizing and internalizing Axis I disorders and gender were tested as potential modifiers of these associations.ResultsFour distinct longitudinal trajectories were identified for both disruptiveness and anxiousness. The high disruptiveness trajectory accounted for the association between childhood adversity and SA, but only for females. The high anxiousness trajectory also explained the association between adversity and SA; however, in this case it was not sex but mental disorders that influenced the potency of the mediating effect. More specifically, anxiousness fully explained the effect of adversity on SA in the presence of externalizing disorders, whereas in the absence of these disorders, this effect was significantly attenuated.ConclusionsThis study provides evidence that both disruptiveness and anxiousness play an important role in explaining the relationship between childhood adversity and SA.

scholarly journals Blunted stress reactivity reveals vulnerability to early life adversity in young adults with a family history of alcoholism

Addiction ◽  
2018 ◽  
Vol 114 (5) ◽  
pp. 798-806 ◽  
Author(s):  
William R. Lovallo ◽  
Andrew J. Cohoon ◽  
Ashley Acheson ◽  
Kristen H. Sorocco ◽  
Andrea S. Vincent
Keyword(s):  
Young Adults ◽  
Family History ◽  
Early Life ◽  
Stress Reactivity ◽  
Early Life Adversity ◽  
History Of

Inflammatory and Epigenetic Pathways for Perinatal Depression

2015 ◽  
Vol 18 (3) ◽  
pp. 331-343 ◽  
Author(s):  
Lindsey Garfield ◽  
Herbert L. Mathews ◽  
Linda Witek Janusek
Keyword(s):  
Early Life ◽  
Infant Health ◽  
Perinatal Depression ◽  
Life Experiences ◽  
Perinatal Period ◽  
Early Life Adversity ◽  
Targeted Interventions ◽  
Increased Risk ◽  
History Of ◽  
The Impact

Depression during the perinatal period is common and can have adverse consequences for women and their children. Yet, the biobehavioral mechanisms underlying perinatal depression are not known. Adverse early life experiences increase the risk for adult depression. One potential mechanism by which this increased risk occurs is epigenetic embedding of inflammatory pathways. The purpose of this article is to propose a conceptual model that explicates the linkage between early life adversity and the risk for maternal depression. The model posits that early life adversity embeds a proinflammatory epigenetic signature (altered DNA methylation) that predisposes vulnerable women to depression during pregnancy and the postpartum period. As proposed, women with a history of early life adversity are more likely to exhibit higher levels of proinflammatory cytokines and lower levels of oxytocin in response to the demands of pregnancy and new motherhood, both of which are associated with the risk for perinatal depression. The model is designed to guide investigations into the biobehavioral basis for perinatal depression, with emphasis upon the impact of early life adversity. Testing this model will provide a better understanding of maternal depressive risk and improve identification of vulnerable women who would benefit from targeted interventions that can reduce the impact of perinatal depression on maternal–infant health.

scholarly journals Hair glucocorticoids are associated with childhood adversity, depressive symptoms and reduced global and lobar grey matter in Generation Scotland

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Claire Green ◽  
Aleks Stolicyn ◽  
Mathew A. Harris ◽  
Xueyi Shen ◽  
Liana Romaniuk ◽  
...  
Keyword(s):  
Hpa Axis ◽  
Life Stress ◽  
Early Life ◽  
Childhood Adversity ◽  
Later Life ◽  
Early Life Adversity ◽  
Brain Volumes ◽  
Stable Measure ◽  
Regional Brain ◽  
Generation Scotland

AbstractHypothalamic–pituitary–adrenal (HPA) axis dysregulation has been commonly reported in major depressive disorder (MDD), but with considerable heterogeneity of results; potentially due to the predominant use of acute measures of an inherently variable/phasic system. Chronic longer-term measures of HPA-axis activity have yet to be systematically examined in MDD, particularly in relation to brain phenotypes, and in the context of early-life/contemporaneous stress. Here, we utilise a temporally stable measure of cumulative HPA-axis function (hair glucocorticoids) to investigate associations between cortisol, cortisone and total glucocorticoids with concurrent measures of (i) lifetime-MDD case/control status and current symptom severity, (ii) early/current-life stress and (iii) structural neuroimaging phenotypes, in N = 993 individuals from Generation Scotland (mean age = 59.1 yrs). Increased levels of hair cortisol were significantly associated with reduced global and lobar brain volumes with reductions in the frontal, temporal and cingulate regions (βrange = −0.057 to −0.104, all PFDR < 0.05). Increased levels of hair cortisone were significantly associated with MDD (lifetime-MDD status, current symptoms, and severity; βrange = 0.071 to 0.115, all PFDR = < 0.05), with early-life adversity (β = 0.083, P = 0.017), and with reduced global and regional brain volumes (global: β = −0.059, P = 0.043; nucleus accumbens: β = −0.075, PFDR = 0.044). Associations with total glucocorticoids followed a similar pattern to the cortisol findings. In this large community-based sample, elevated glucocorticoids were significantly associated with MDD, with early, but not later-life stress, and with reduced global and regional brain phenotypes. These findings provide important foundations for future mechanistic studies to formally explore causal relationships between early adversity, chronic rather than acute measures of glucocorticoids, and neurobiological associations relevant to the aetiology of MDD.

scholarly journals Association of BDNF Val66Met Polymorphism and Brain BDNF levels with Major Depression and Suicide

2017 ◽  
Author(s):  
Mariam M. Youssef ◽  
Mark D. Underwood ◽  
Yung-Yu Huang ◽  
Shu-chi Hsiung ◽  
Yan Liu ◽  
...  
Keyword(s):  
Major Depression ◽  
Early Life ◽  
Childhood Adversity ◽  
Anterior Cingulate ◽  
Bdnf Expression ◽  
Early Life Adversity ◽  
Val66met Polymorphism ◽  
Protein Levels ◽  
Dorsolateral Prefrontal ◽  
Bdnf Val66met Polymorphism

ABSTRACTBrain-derived neurotrophic factor (BDNF) is implicated in the pathophysiology of major depressive disorder (MDD) and suicide. Both are partly caused by early life adversity (ELA) and ELA reduces both BDNF protein and gene expression. This study examines the association of BDNF Val66Met polymorphism and brain BDNF levels with depression and suicide. We hypothesized that both MDD and ELA would be associated with the Met allele and lower brain BDNF levels. Such an association would be consistent with low BDNF mediating the effect of ELA on adulthood suicide and MDD. BDNF Val66Met polymorphism was genotyped in postmortem brains of 37 suicide decedents and 53 non-suicides. Additionally, BDNF protein levels were determined by Western blot in dorsolateral prefrontal cortex (Brodmann area 9; BA9), anterior cingulate cortex (ACC; BA24), caudal brainstem and rostral brainstem. The relationships between these measures and major depression, death by suicide and reported childhood adversity were examined. Depressed subjects had an excess of the Met allele and lower BDNF levels in ACC and caudal brainstem compared with non-depressed subjects. No effect of history of suicide death or early life adversity was observed with genotype, but lower BDNF levels in ACC were found in subjects who had been exposed to early life adversity and/or died by suicide compared to nonsuicide decedents and no reported childhood adversity. This study provides further evidence for low BDNF in major depression related to the BDNF met risk allele. Future studies should seek to determine how altered BDNF expression contributes to MDD and suicide.

Unbiased Screening Identifies Functional Differences in NK Cells After Early Life Psycho-Social Stress

2021 ◽  
Author(s):  
Sara B. Fernandes ◽  
Neha D. Patil ◽  
Sophie B. Meriaux ◽  
Maud Theresine ◽  
Fleur A.D. Leenen ◽  
...  
Keyword(s):  
Immune System ◽  
Immune Responses ◽  
Nk Cells ◽  
Early Life ◽  
Social Stress ◽  
Maternal Separation ◽  
Economic Status ◽  
Childhood Adversity ◽  
Early Life Adversity ◽  
Human Situation

Early Life Adversity (ELA) is closely associated with the risk for developing diseases later in life, such as autoimmune diseases, type-2 diabetes and cardiovascular diseases. In humans, early parental separation, physical and sexual abuse or low social-economic status during childhood are known to have great impact on brain development, in the hormonal system and immune responses. Maternal deprivation (MD), the closest animal model available to the human situation, is known to similarly induce long lasting behavioural effects, to cause changes in the HPA axis and to have an impact in the immune system. Even though the immune responses to potential pathogens after early stress have been somehow documented, the mechanisms by which they occur are still not fully understood. Here, we have demonstrated that maternal separation, in both humans and rats, significantly affects the sensitivity of the immune system in adulthood. Particularly, NK cells&rsquo; profile and response to target cell lines are significantly changed after childhood adversity. These immune cells in rats are not only less cytotoxic towards YAC-1 cells, but also show a clear increase in the expression of maturation markers after 3h of maternal separation. Similarly, individuals who suffered from ELA display significant changes in the cytotoxic profile of NK cells together with decreased degranulation capacity. Altogether, these results lead us to conclude that one of the key mechanisms by which the immune system becomes impaired after ELA might be due to a shift on the senescent state of the cells, specifically NK cells. Elucidation of such a mechanism highlights the importance of ELA prevention and how NK targeted immunotherapy might help attenuating ELA consequences.

scholarly journals On the early-life origins of vulnerability to opioid addiction

2019 ◽  
Author(s):  
Sophia C Levis ◽  
Brandon S Bentzley ◽  
Jenny Molet ◽  
Jessica L Bolton ◽  
Christina R Perrone ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Brain Development ◽  
Early Life ◽  
Opioid Addiction ◽  
Opioid Abuse ◽  
Female Rats ◽  
Early Life Adversity ◽  
History Of ◽  
And Function ◽  
Reward Circuit

AbstractThe origins and neural bases of the current opioid addiction epidemic are unclear. Genetics plays a major role in addiction vulnerability, but cannot account for the recent exponential rise in opioid abuse, so environmental factors must contribute. Individuals with history of early-life adversity (ELA) are disproportionately prone to opioid addiction, yet whether ELA interacts with factors such as increased access to opioids to directly influence brain development and function and cause opioid addiction vulnerability is unknown. We simulated ELA in female rats and this led to a striking opioid addiction-like phenotype. This was characterized by resistance to extinction, increased relapse-like behavior, and, as in addicted humans, major increases in opioid economic demand. By contrast, seeking of a less salient natural reward was unaffected by ELA, whereas demand for highly palatable treats was augmented. These discoveries provide novel insights into the origins and nature of reward circuit malfunction that may set the stage for addiction.

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