Pregnancy alcohol consumption has been linked to poor birth outcomes and long-term developmental problems. Despite this, a significant number of women drink during pregnancy. Although most prenatal care providers are asking women about alcohol use, validated screening tools are infrequently employed. Research has demonstrated that currently available screening methods and intervention techniques are effective in identifying and reducing pregnancy drinking. Implementing universal screening and appropriate intervention for pregnancy alcohol use should be a priority for prenatal care providers, as these efforts could substantially improve pregnancy, birth, and longer term developmental outcomes for those affected.

Ph.D., Faculty of Health Sciences, University of the Witwatersrand, 2011 / Fetal Alcohol Spectrum Disorder (FASD) is a preventable cause of intellectual delay. Highly prevalent in South Africa, it has become a public health concern. Effective screening measures to identify women at risk of producing a FASD child is therefore important. This study postulated that a distinctive maternal profile may exist for mothers with FASD infants compared to a comparison group. Consequently, the study investigated the occurrence of maternal depression and its potential association with maternal risk factors and infant development respectively; differences in the profiles of mothers; as well as developmental differences in FASD and No FASD groups of children. An ex-post facto design was implemented, where the sample comprised of dyads that completed initial (infants 9-18 months) and follow-up (children 18-45 months) assessments. Severity of maternal depression (measured on the Beck Depression Inventory); maternal current mood states (measured on the Profile of Mood States) and infant developmental differences (measured with the Griffiths Mental Developmental Scales) were assessed. The results showed no distinct patterns in maternal depression in the FASD versus the No FASD groups; maternal depression was not significantly correlated with infant development; infants with FASD showed impaired overall development, with especially poor social adjustment; and all infants (FASD and No FASD) performed lower than the expected developmental norms. Maternal alcohol use was the only significant covariate associated with infant development. Identifying the predictors of high risk behaviour during pregnancy is complex, where prenatal alcohol exposure cannot be viewed in isolation from contextual factors, as limited resources, historical factors, cultural/community knowledge, a lack of stimulation and malnutrition prevail in many areas of South Africa. Profiling maternal predisposition to prenatal alcohol use is essential in reducing the incidence of FASD in South Africa and implementing social skills intervention programs could aid the long-term adjustment of FASD infants.

Student Number : 0416521T - MSc(Med) dissertation - School of Pathology - Faculty of Health Sciences / Fetal alcohol spectrum disorder (FASD) encompasses a range of conditions induced by prenatal alcohol exposure. Fetal alcohol syndrome (FAS) is the most severe of these conditions. FAS is characterised by discriminating facial features along with growth deficiencies and central nervous system abnormalities. FASD is a growing concern in South Africa, particularly in the Northern and Western Cape Provinces. In the Northern Cape, astounding prevalence rates of 122 and 73.8 per 1000 school entry children have been established for the towns of De Aar and Upington respectively. Studies involving twin concordance research and animal models have indicated that there is a genetic influence contributing towards FAS susceptibility in individuals. FAS is considered a complex disease whereby both genetic and environmental factors interact in disease pathogenesis. For this reason a case-control study involving the investigation of appropriate candidate genes was conducted. The neuronal migration pathway in the developing brain is targeted by prenatal alcohol exposure. The astrotactin (ASTN) and reelin (RELN) genes were selected for investigation based on their fundamental role in neuronal migration. A FAS case-control study involving 45 cases and 112 controls was conducted on the Northern Cape Coloured population. Four single nucleotide polymorphisms (SNPs) including missense and non-coding variants were selected within ASTN and four missense SNPs were selected within RELN. The study aimed to determine the genotype and allele frequencies of the variants within the case and control groups and to assess whether any association between the gene variants and the predisposition to FAS existed. Statistical analyses indicated a significant genotypic association (P= 0.049) between RELN’s rs607755 marker; the C/T genotype was more likely to be found amongst controls thus inferring a possible protective effect against FAS. A logistic regression model supported the above association by indicating the C/T genotype as being independently significant (P= 0.026). The most limiting factor of this study was the small sample size and consequent lack of power to detect genes with minor effects. It would therefore be suggested that the study be repeated once a larger sample size has been established. A larger sample size would increase the chances of detecting true associations between genes of minor effect and FAS, thus minimising false-positive associations from arising.

While accounting for less than 5 percent of the Canadian population, Indigenous peoples represent more than 30 percent of the federal prison population of Canada. In a prairie province like Manitoba the numbers are even more extreme, with over three-quarters of the prison population being Indigenous. This contemporary “Indian Problem” has been theorized in recent decades as an outcome of the colonial history of Canada. Indigenous Studies scholarship has critiqued the temporal political imaginary of the subsequent reconciliation discourse that locates colonial violence, and, thus, culpability and responsibility of the Canadian state, to an ‘event’ of history. Such national stories not only diminish the interrogation of ongoing structures of colonial violence but relegate any meaningful political processes of accountability and justice to the dustbin of history. This ‘legacy’ framework of historicizing colonial violence has created fecund conditions for (re)apprehending Indigenous bodies at the junctures of legal and medical reasoning, where questions of punishment, containment and rehabilitation for criminal actions become uneasily blurred with questions of healing and repair of damaged bodies and minds. The uptake of ‘Fetal Alcohol Spectrum Disorder’ (FASD) in the Canadian justice system in recent decades operates precisely at this juncture of treating Indigenous peoples as uniquely medicalized, or disabled, criminals, and has created further capacities for deepening this ‘legacy’ framework for apprehending and containing Indigenous peoples as offenders, or even as potential offenders of a social and legal order. FASD is an umbrella term describing the range of lifelong physical, mental, behavioral and learning disabilities that can occur in an individual who was exposed to alcohol while in utero. It is typically thought of as a neurocognitive disability that affects memory, executive reasoning, and the ability to learn from or think consequentially about one’s actions. As such, it has become a broad institutional discourse for predicting criminal behaviors through a medicalized conception of risk of violence. FASD is typically raised as an ethical problem in the criminal justice system, provoking important questions as to whether we punish crimes (for which one is culpable) or disabilities (for which one is not). In addition, if FASD represents a permanent neurocognitive disability without any hope of cure, how should the rehabilitative and reintegrative tenets of the criminal code be imagined and implemented? These problems are compounded further by the regular speculation that Canada is in the midst of a hitherto unknown epidemic of this “invisible disorder” of FASD. Important as these ethical and political problems are, the dissertation argues that the specific institutional urgency surrounding the medicalization of criminal offenders with FASD has been enabled by diagnostic logics of deferral and certainty that pertains to the “Indian Problem.” These logics allow FASD to relocate and bury questions of colonial responsibility within the Indigenous body itself which is tragically doomed to permanent brain damage and cognitive disorder and an incorrigible lifestyle of dysfunction and crime. The ‘colonial legacy’ predicates a foreclosure on Indigenous futurity. This dissertation is based on 24 months of fieldwork in a non-profit community outreach program for justice-involved individuals with FASD in Winnipeg, Manitoba. As an FASD community outreach worker, my job was to assist individuals to navigate the complexities of criminal justice and social welfare systems that might pose challenges to those with cognitive disabilities associated with FASD. I learned very quickly, however, that actors as diverse as lawyers, probation officers, doctors, social workers, FASD researchers and even my community outreach colleagues and supervisors, operated within a diagnostic imaginary that quite often assumed without proof the presence of an FASD diagnosis for our almost exclusively Indigenous clientele. The dissertation analyzes the everyday procedures of FASD knowledge formation and circulation beginning with a basic ethnographic question: how does one know that another has FASD? This line of questioning was situated within the broad institutional apparatus of the criminal justice system in Canada, which I examine thematically and temporally as four separate stages of encounter: 1) the initial crime and related discourses of accusation; 2) the trial setting; 3) the sentencing trial; and, finally, 4) the post-carceral release phase. This temporal framework emerged naturally out of my experience of ethnographic work as a community outreach worker and innumerable casual and professional encounters with social workers, slum landlords, and my many hours spent in courts, probation offices, and jail visitations. In addition, I had a four-month placement with an assessment team at an FASD diagnostic clinic and did extensive work in the archive of legal cases and decisions pertaining to Indigenous offenders and the unique problematic of FASD in the legal system. Breaking down the minute social and legal details that attend to determinations of FASD at these various stages unmasks the ways in which FASD comes to explain Indigenous criminality as a congenital condition that is an expression of biological and cultural dysfunction, while strategically ignoring any examination of ongoing structures of colonial violence.

Pattern formation ensures that tissues, organs, and structures develop in the correct place and orientation within the body. Patterning processes are at the heart of morphogenesis yet remain poorly understood due to their complexity. The sea urchin larval skeleton provides a simple model to study skeletal patterning, where the skeleton-producing primary mesenchyme cells (PMCs) receive patterning cues from the overlying ectoderm. The normal skeletal patterning process requires the PMCs to migrate within the blastocoel to specific positions. While ectodermal and endodermal signals regulate PMC positioning and differentiation, additional signals act to regulate biomineralization per se in the PMCs. However, the distinction between these effects is not well understood and new efforts have been made to identify these patterning and biomineralization cues that regulate sea urchin skeletal development. Understanding the mechanism by which PMCs interpret and transduce patterning cues into a migratory bias and/or positional information will provide insight into tissue patterning and developmental plasticity both in sea urchins and, more broadly, in deuterostomes. Ethanol is a known vertebrate teratogen that causes craniofacial defects as a component of fetal alcohol syndrome. Perturbations to retinoic acid biosynthesis and the Hedgehog signaling pathway are thought to be causal for the fetal alcohol syndrome phenotype in vertebrates. We used the sea urchin embryo to gain evolutionary insight into how ethanol affects embryonic development in a basal deuterostome animal. We found that ethanol specifically perturbs skeletal patterning. When sea urchin embryos are exposed to ethanol, they exhibit conspicuously delayed development, and broad skeletal patterning defects that are potentially analogous to fetal alcohol syndrome associated facial patterning defects in vertebrates and humans. PMC transplantation experiments demonstrated that ethanol-induced defects are not specific to the PMCs, and instead reflect the perturbation of patterning cues. We also found that the expression of both patterning cues and PMC-specific genes was delayed by ethanol exposure. Surprisingly, our results indicate that retinoic acid and Hedgehog pathways are not functionally relevant for the teratogenic effects of ethanol in the larval skeletal patterning process, indicating a lack of evolutionary conservation of these pathways in ethanol-mediated teratogenesis among deuterostomes. Temporal transcriptome analysis revealed significant impacts of ethanol on signaling and metabolic gene expression and a disruption in the timing of expression for sea urchin specification gene regulatory network (GRN) genes. Surprisingly, multiple circuits with the GRN exhibit precocious expression while others are delayed. Taken together, our results suggest that the skeletal patterning perturbations in ethanol-treated sea urchin embryos arise from a loss of temporal synchrony within and between the instructive and responsive tissues during pattern formation.

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An animal model (Rattus norvegicus) was employed to study the effects of chronic prenatal alcohol exposure on pup development and on the functional efficacy of pup vocalizations on the maternal behavior of the dam. Subjects were 72 dams and their litters. Dams were matched by weight and assigned to either an Ethanol (EtOH), a Pair-fed (PF), or an Untreated Control (UC) group. Ethanol dams received 15% ethanol as their sole source of fluid throughout the experiment. Pair-fed dams were fed isocalorically to EtOH dams. Untreated Control dams received food and water ad libitum. Dam's retrieval behavior was assessed in a runway choice situation when pups were 3, 5, 7, and 9 days old. Developmental measures were taken on pups from ages 0 through 13 days. Blood ethanol concentrations were also analyzed for dams and pups. The data showed that the BEC of EtOH dams was .1% and that EtOH pups showed a negligible BEC postpartum. Prenatal alcohol exposure was shown to have a direct pharmacological and indirect nutritional effect on pup development. Ethanol dams retrieved a reliably smaller percentage of pups and retrieved reliably more slowly than did controls. Pair-fed pups showed a higher rate of calling than did other pups and tended to be chosen more often by UC and PF dams than were EtOH or UC pups. Ethanol dams tended to chose UC pups more often than other pups. These findings suggest that chronic prenatal alcohol exposure produces altered behavior and responsiveness in the dam and the pup. This altered behavior and responsiveness may have a synergistic effect on the interaction between the dam and the pup. / Master of Science

Thesis (MEdPsig)--University of Stellenbosch, 2006. / ENGLISH ABSTRACT: The research in this qualitative study focuses on the role of the Educational Psychologist in facilitating inclusion of a learner with Fetal Alcohol Syndrome (FAS). The international movement towards inclusive education, with emphasis on the inclusion of all learners irrespective of their special needs in mainstream schools, gained momentum in the South African context with the announcement of Education White Paper 6, Special Needs Education: Building an Inclusive Education and Training system. More learners with FAS are accommodated in mainstream schools and research has indicated that most cases of FAS in the world prevailed in the Western Cape. FAS is one of the leading causes of mental retardation and the challenges which the inclusion of learners with FAS pose to those who have to facilitate inclusive education, has urged this study. The study seeks to explore the role of the Educational Psychologist in the process of facilitating inclusion of a learner with FAS. An eco-systemic approach underpins the study. A single learner with FAS within the context of the family and education system was chosen by means of purposive sampling as the focus of a qualitative, case study. The eco-systemic approach makes it possible to explore special needs in terms of intrinsic factors (within the learner) and extrinsic factors (within the system) in order to address the needs of the system. Semistructured interviews were held with respondents from different levels of the eco-system in which the learner functions. A review of personal records and field notes were used to gather information related to the education and learning process. The data were analysed using aspects of content analyses. Four themes emerged: support to the learner, support to the school, support to the parents and support to the school community. The findings indicated that the inclusion of learners with FAS predicts a change and an expansion in the role of the educational psychologist. Early identification, early intervention and a multi-functional team approach seem to improve the long-term prognoses of learners with FAS. The facilitation of inclusive education for learners with FAS poses a challenge to the educational psychologist to render individual support, but also to provide support in a holistic systemic manner, focusing on those who work and live with the individual learners. The learning, behaviour and developmental barriers which learners with FAS may experience were highlighted with the hope to guide those who work with these learners. Several positive and negative factors were indicated and recommendations were made. / AFRIKAANSE OPSOMMING: Hierdie kwalitatiewe studie fokus op die rol van die Opvoedkundige Sielkundige in die fasilitering van inklusiewe onderwys aan 'n leerder met Fetale Alkohol Sindroom (FAS). Die internasionale beweging na inklusiewe onderwys, wat die insluiting van alle leerders, ongeag hulle spesiale behoeftes, by hoofstroomskole onderskryf, het ook in Suid-Afrika neerslag gevind met die uitreiking van die Onderwys Witskrif 6, Special Needs Education: Building an Inclusive Education and Training System. Meer leerders met FAS word by hoofstroomskole ingesluit en navorsing het getoon dat die voorkomssyfer van FAS in die Wes-Kaap die hoogste ter wêreld is. Die feit dat FAS tans een van die vernaamste oorsake van verstandelike gestremdheid is, en die uitdagings wat die insluiting van leerders met FAS aan diegene wat inklusiewe onderwys moet fasiliteer bied, het hierdie navorsingsondersoek genoop. Die doel van hierdie studie is om 'n in diepte ondersoek te doen na die rol van die Opvoedkundige Sielkundige in die fasilitering van inklusiewe onderwys aan 'n leerder met FAS. 'n Ekosistemiese benadering het die teoretiese raamwerk van die studie gevorm. 'n Enkele leerder met FAS is binne die konteks van sy familie en die onderwyssisteem, met behulp van doelgerigte steekproefneming, gekies om die fokus van die kwalitatiewe gevallestudie te vorm. Die ekosistemiese benadering maak dit moontlik om spesiale behoeftes ten opsigte van faktore wat primêr by die leerder (intrinsiek) voorkom, sowel as faktore wat in die sisteem (ekstrinsiek) voorkom, te ondersoek en te verseker dat die behoeftes van die sisteem aangespreek word. Semi-gestruktureerde onderhoude is gevoer met respondente uit die verskillende vlakke van die ekosisteem waarbinne die leerder funksioneer. 'n Oorsig van persoonlike rekords en verslae asook veldnotas is gebruik om inligting oor die leerder, die onderrig en die leerposes te bekom. Inhouds-analise is gebruik om die data te analiseer. Vier temas het uit die data na vore gekom, naamlik: ondersteuning aan die leerder, ondersteuning aan die skool, ondersteuning aan die ouers en ondersteuning aan die skoolgemeenskap. Die bevindinge dui daarop dat die insluiting van 'n leerder met FAS 'n roluitbreiding en 'n veranderende rol vir die Opvoedkundige Sielkunde in die vooruitsig stel. Vroeë identifikasie, vroeë intervensie en 'n multi-funksionele spanbenadering kan die langtermyn prognose van leerders met FAS verbeter. Die rol wat die Opvoedkundige Sielkundige op die verskillende vlakke van die ekosisteem kan speel, ten einde inklusiewe onderwys aan 'n leerder met FAS te fasiliteer, lê opgesluit in die mate waarin geïndividualiseerde, maar tog ook holisties omvattende ondersteuning aan diegene wat met hierdie leerders werk, gelewer kan word. Uit die bevindinge het suksesvolle en minder suksesvolle aspekte duidelik geword. Dit het daartoe bygedra dat die leer-, gedrag- en ontwikkelingshindernisse, sowel as die sterkpunte van die leerder met FAS, duidelik geword het en wenke vir toekomstige gebruik verbesonder kon word. Op grond van die bevindinge en aan die hand van literatuur is aanbevelings gemaak.

OF THE THESIS Name: Bc. Petra Symonová Specialization: Adiktologie Head of the thesis: Mgr. Lenka Šťastná, PhD. Pages: 77 The name of thesis: Alcohol use during pregnancy. Prevalence and awareness of the harmful effects of alcohol use in pregnant women - clients of the Institute for Mother and Child in Prague. Abstract: Background: With the increasing trend of alcohol use in a population, but also increases the number of women who are dependent on alcohol in pregnancy. Since your problem but ashamed and fears of condemnation of the behavior of companies admit the problem and continued to try to hide it, and therefore it is not possible to quickly capture and begin to solve. Alcohol consumed during pregnancy the mother may hurt not only her but also her fetus. Since we do not know the exact amount that is 'safe' should be gynecologists recommended total abstinence. This fact, however, in many cases, unfortunately, beyond reality. Goals: The main objective of this work was to determine the prevalence of alcohol use among pregnant women. Other objectives were to determine what are the knowledge of pregnant women about alcohol use in pregnancy, where and whether they are informed of pregnant women about the harmful effects of alcohol use during pregnancy and to determine whether the health of the fetus...

In the context of fetal alcohol spectrum disorders, we investigated how the nitric oxide (NO) signaling pathway influences intracellular calcium (Ca2+) to mediate alcohol resistance, using a primary cell culture model of cerebellar granule neurons (CGN). Alcohol during fetal brain development triggers abnormally high apoptotic cell death in vulnerable neuronal populations, culminating in serious behavioral and cognitive deficits that persist into adulthood. Prior studies demonstrated that the NO signaling pathway [neuronal nitric oxide synthase → NO → soluble guanylyl cyclase → cyclic guanosine monophosphate → protein kinase G (PKG)] mitigates alcohol toxicity, consequently diminishing neuronal loss both in vivo and in vitro. Endoplasmic reticulum (ER) Ca2+ release, a key apoptotic mechanism, requires the inositol 1,4,5-trisphosphate receptor (IP3R), a known PKG substrate. Our studies focused on this crucial intersection point where the NO signaling cascade can influence Ca2+-mediated apoptotic mechanisms, and exposed a downstream mechanism where NO can moderate alcohol neurotoxicity. We hypothesized that as alcohol disturbs neuronal Ca2+ homeostasis to trigger cell death, the NO signaling pathway counters it by limiting Ca2+ release from the ER. We examined first the role of the phospholipase C (PLC) pathway [PLC → inositol 1,4,5-trisphosphate → IP3R → Ca2+] in developmental neurotoxicity through our in vitro CGN model, extending previous in vivo studies. We found that alcohol terminates developing neurons by eliciting abnormal Ca2+ release from the ER rather than from an extracellular source, via a PLC - IP3R-dependent signaling mechanism. Inhibiting either calcineurin or Ca2+ / calmodulin-dependent protein kinase ii (CaMKii), which participate in parallel Ca2+-activated apoptotic cascades, shielded CGN cultures from alcohol. Blocking the mitochondrial Ca2+ uniporter or the mitochondrial permeability transition pore also provided neuroprotection. That the activated pathways must interact to generate cell death likely explains why inhibiting one of multiple parallel signaling cascades limits alcohol toxicity. We next demonstrated that activating the NO pathway downstream at PKG eliminated both alcohol-related neuronal death and the accompanying rapid rise in intracellular Ca2+, an effect that markedly resembled IP3R inhibition. Experiments that temporally manipulated the addition of PKG activators in relation to alcohol exposure linked PKG's obstruction of alcohol-induced Ca2+ elevations to alcohol resistance. In contrast, brain-derived neurotrophic factor (BDNF), which does not rely on PKG to provide neuroprotection, failed to block alcohol-induced Ca2+ elevations while preventing alcohol toxicity. This indicates that although PKG blocks alcohol-induced Ca2+ elevations, averting these Ca2+ elevations is not necessary for neuroprotection. BDNF may confer alcohol resistance through an as yet unidentified process downstream from the disruption of intracellular Ca2+. In summary, we established that 1) alcohol induces toxic Ca2+ elevations originating from the ER through a PLC - IP3R-dependent pathway, and that 2) PKG-mediated alcohol resistance is linked to preventing the intracellular Ca2+ surges. These findings support the hypothesis that the NO signaling pathway shields developing neurons from alcohol by limiting Ca2+ release from the ER.