This study investigated the effect of chronic alcohol exposure on the responses of the maternal hypothalamus-pituitary adrenal axis (HPA-axis) and thyroid hormones throughout gestation using an ovine model. Maternal plasma concentrations of ACTH, cortisol and the thyroid hormones T3, free T4 and total T4 were determined in response to infusion of 0.75, 1.25 and 1.75 g/kg alcohol. Maternal endocrine responses to alcohol administration have been investigated before in rodent models. However, this is the first study using a large animal model (sheep), in which all three human trimester equivalents occur in utero. Different concentrations of alcohol were administered intermittently from gestational day 4 to 132 in a pattern that modeled human binge drinking during pregnancy. Maternal blood samples were collected on specific days (GD 6, 40, 90, 132) and at multiple time-points (0, 0.5, 1, 1.5, 2, 6, 24 hours) and were analyzed to determine blood alcohol concentrations (BACs) and ACTH, cortisol, free T4, total T4 and T3 plasma concentrations. Alcohol readily permeates the placenta and can directly affect fetal cells and tissues. Alcohol also causes endocrine imbalances in the mother and interferes with maternal-fetal hormonal interactions and the mother’s ability to maintain a healthy pregnancy, thus also indirectly affecting fetal development. Sheep receiving either 0.75, 1.25 or 1.75 g/kg alcohol achieved peak BAC values of 93 + 5, 126 + 5 and 183 + 5 respectively. Alcohol exposure resulted in increased plasma ACTH and cortisol concentrations peaking at 2 hours after beginning of the infusion and returning to baseline values at 6 hours after beginning of the infusion. There was no effect of alcohol on any of the plasma thyroid hormone concentrations. Thyroid hormone concentrations changed as a result of progressing pregnancy. Plasma concentrations of total T4 and free T4 were higher on gestational days 6 and 40 compared to GDs 90 and 132, and plasma T3 concentrations were highest on GD 6. The results of this study show that alcohol stimulates the HPA-axis in a dose dependent fashion in pregnant sheep. The response of the HPA-axis to repeated alcohol exposure throughout gestation remained unchanged. Alcohol exposure did not affect the release of thyroid hormones. Thyroid hormone concentrations changed during pregnancy in sheep in a manner similar to changes observed in pregnant women.

Thesis (Ph.D.)--Brown University, 2008. / Vita. Advisor : Suzanne M. de la Monte. Includes bibliographical references.

Northern British Columbian Aboriginal mothers raising adolescents with Fetal Alcohol Spectrum Disorder (FASD) face many challenges. This interpretive ethnography provides an understanding of how these mothers interpreted and responded to their adolescents' FASD. It affirms the experiences of Aboriginal mothers and acknowledges their life stories and those of their adolescent children.The concepts of vulnerability, marginalization, and mothering, conceptualized within the theoretical perspectives of postcolonialism, provided the framework for this study. Postcolonial perspectives were particularly relevant to this research: the explicit aftereffects of colonialism on the well-being of Aboriginal women have shaped the worldview of mainstream society resulting in marginalization and stigmatization. A postcolonial perspective suggests that FASD is a problem compounded by colonization; until the underlying compounding issues are addressed, the incidence of FASD among Aboriginal people will continue to increase.English-speaking Aboriginal women with one or more children between the ages of 14 and 18 years affected by FASD were recruited for the study. Appropriate measures were taken to ensure trustworthiness, verisimilitude, and legitimacy. Data collection included three sequential audio-recorded interviews with eight women over a specific time. Interview data were enhanced by document review, intervals of observation participation, and the examination of other historically and culturally relevant data.The interpretive theory derived from the data, Mothering from the Margins, explains how Aboriginal mothers raise their adolescent children who have FASD. The theory provides a perspective that enables nurses to view mothers with adolescents affected by FASD in an all-encompassing manner, and unifies the experiences of participants mothering adolescents with FASD. Aboriginal mothers of adolescents with FASD continue to experience societal blame and marginalization for consuming alcohol during pregnancy. This study extends the knowledge of how this blaming and marginalization experience plays out in the lives of both mothers and children. The findings debunk the stereotypical myth that Aboriginal mothers are not good mothers. In fact, the findings from this study demonstrate how, despite all the difficulties and challenges faced by study participants, they have demonstrated adaptability, confidence, and care in their mothering roles.

In this thesis I used Caenorhabitis elegans as a model of Fetal Alcohol Spectrum Disorder (FASD) to study the physical and behavioral effects of ethanol exposure during embryonic development. Davis et al. (2008) found that ethanol exposure during larval development in C. elegans produced physical/developmental and behavioral effects; however, whether exposure during embryonic development might produce similar outcomes remained to be elucidated. Because the type and degree of effects caused by developmental ethanol exposure was dependent on the pattern of ethanol treatment, in the first part of the thesis I investigated the physical/developmental effects of embryonic exposure to various ethanol doses, exposure durations, onsets and frequencies. I found that exposure to >30% ethanol for an hour during embryonic development was necessary to lower hatch rate, delay reproductive onset, and reduce body size in C. elegans. Furthermore, exposure during early embryonic development caused a larger effect than exposure during later stages, and multiple exposures produced a worse outcome than a single exposure for a comparable duration. In the second part of the thesis, I investigated locomotory activities and habituation of adult C. elegans exposed to various patterns of embryonic ethanol treatment. I found that the rate of locomotion was altered differently by chronic and acute embryonic ethanol exposure, but I did not find any effect in short- or long-term habituation. In summary, I have characterized the pattern of embryonic ethanol exposure necessary to produce physical/developmental effects in C. elegans, and identified the types of exposure conditions that would cause worse outcomes than others; in addition, I have found that embryonic ethanol exposure affects the rate of locomotion in C. elegans. In this thesis, I have established a foundation for the future investigation into the physical and motor defects caused by embryonic ethanol exposure in C. elegans.

The current document is a paper-based thesis investigating the lived experiences of parents raising children with Fetal Alcohol Spectrum Disorder (FASD) in Ontario, Canada. Historically, researchers have approached the exploration of families with the notion that families of children with a developmental disability would present with a pathological profile. However, a recent paradigm shift has transitioned the focus from deficit-based outcomes to those that highlight positive outcomes. Therefore, the first paper included is a qualitative analysis of factors that facilitate family adaptation. Interpretative phenomenological analysis (IPA) was used to analyze semi-structured interviews with parents of children with FASD. Parents utilize a number of coping strategies, supports, and transformational outcomes that enable them to adapt to raising their child with FASD. The second paper included is also a qualitative analysis examining demands that hinder family adaptation. Parents discussed five stressors that hinder successful family adaptation. Recommendations from parents of children with FASD and implications for increasing knowledge and awareness of the disability are discussed.

This research explored the risk and protective factors associated with criminality among adults with Fetal Alcohol Spectrum Disorder (FASD). While previous research has focused on identifying the factors that contribute to legal issues, there is a paucity of research on the protective factors that may lead to more positive outcomes for adults with FASD. The first paper examined the methodological issues encountered while conducting a mixed methods study on the experience of offenders and non-offenders with FASD. Difficulties with participant recruitment, the sample size, the terminology employed, and the appropriateness of psychometric measures were significant challenges that emerged during the research project. The second paper was a qualitative study that investigated the experience of adults with prenatal alcohol exposure and their families to determine the risk and protective factors for criminality. Families reported that neurobehavioural impairments such as difficulty with self-regulation and social skills deficits, combined with environmental demands that exceeded the capabilities of the individual with FASD, were important contributors to criminality. However, structure and supervision, education and employment, social and financial support, and positive peer influence were found to mitigate the risk of criminal behavior among adults with FASD. The findings from this thesis highlight the importance of including families in the research process as well as the need to have more family-centered services.

No description available.

Background: Prenatal alcohol exposure causes behavioural, growth and central nervous system deficits in the offspring, termed Fetal Alcohol Spectrum Disorder (FASD). Our lab has previously shown that structured saccadic eye movement tasks probe executive functioning and can be used to measure cognitive dysfunction in children with an FASD, because performance of these tasks reflects the structural integrity of brain areas shown to be vulnerable to prenatal alcohol exposure. Recently developed portable electroencephalographic (EEG) devices record brain activity using a single dry-sensor electrode. Our objectives were: 1) to assess attention and working memory via a delayed memory-guided saccadic eye movement task of varying mnemonic load and 2) to explore the use of a portable single-channel EEG recording device in measuring differences in frontal lobe activity in children with FASD during the performance of this eye movement task. Methods: A total of 18 children with an FASD diagnosis and 19 typically developing control children performed a memory-guided saccadic eye movement task with one, two or three target stimuli. During the task, frontal lobe EEG was recorded using the Neurosky Mindwave Mobile® portable recording device. Results: In the delayed, memory-guided task when two or three target stimuli were required to be held in working memory, children with an FASD performed the task correctly less often than children in the control group. During task performance, children with FASD exhibited a reduction in theta frequency band power, and in alpha frequency band power only at higher mnemonic loads, suggesting that children with FASD recruited more cognitive resources to complete the task. Conclusion: The results of this study suggest that a portable EEG recording device can be used to assist in the recognition of underlying neural mechanisms of executive functioning deficits in children with FASD. Portable devices offer greater user comfort than typical EEG recording equipment as well as flexibility for use outside the laboratory. This could greatly facilitate the study of children with FASD, and other groups who may be less tolerant of typical laboratory environments. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2013-08-14 20:22:10.995

Developmental ethanol exposure causes both structural and functional changes in the brain that can result in cognitive and behavioral abnormalities. The hippocampal formation, an area of the brain strongly linked with learning and memory, is particularly vulnerable to the teratogenic effects of ethanol. Research in this thesis focused on uncovering the effects of developmental ethanol exposure on hippocampal function in adulthood, particularly synaptic plasticity (a putative neurobiological mechanism of learning and memory). The first experiment sought to determine the temporal vulnerability of hippocampal synaptic plasticity as a function of exposure to ethanol during a single trimester. Ethanol exposure during the 1st or 3rd trimester equivalent resulted in minor changes in synaptic plasticity in adult offspring. In contrast, ethanol exposure during the 2nd trimester equivalent resulted in a pronounced decrease in long-term potentiation (LTP), indicating that the timing of exposure determines the severity of the deficit. The second experiment was aimed at determining the effects of prenatal ethanol exposure (1st and 2nd trimester equivalent combined) on bidirectional synaptic plasticity. Prenatal ethanol exposure resulted in a profound reduction in LTP but did not affect long-term depression. These findings show that prenatal ethanol exposure creates an imbalance in bidirectional synaptic plasticity. The third experiment sought to determine if prenatal ethanol exposure alters the affect of acute ethanol exposure in adulthood on synaptic plasticity. Acute exposure to ethanol in adulthood attenuated LTP in control offspring. Conversely, the magnitude of LTP was not affected by acute ethanol application in prenatal ethanol offspring. These results suggest that prenatal ethanol exposure alters the physiological response to ethanol in adulthood. Together, the results from the experiments undertaken in this thesis demonstrate long-lasting alterations in synaptic plasticity as the result of developmental ethanol exposure. Furthermore, these results allude to a malfunction of neural circuits within the hippocampal formation, perhaps relating to the learning and memory deficits observed in individuals with fetal alcohol spectrum disorders. / Graduate

Thesis (Ph. D.)--University of Hawaii at Manoa, 2004. / Includes bibliographical references (leaves 92-105). / Also available by subscription via World Wide Web / xv, 105 leaves, bound ill. 29 cm