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The Novartis Foundation Series is a popular collection of the proceedings from Novartis Foundation Symposia, in which groups of leading scientists from a range of topics across biology, chemistry and medicine assembled to present papers and discuss results. The Novartis Foundation, originally known as the Ciba Foundation, is well known to scientists and clinicians around the world.
Recognition of the relationship between alcohol abuse and adverse prenatal outcomes is reflected in the warning labels on every alcoholic beverage sold in the United States. Because alcohol abuse has serious consequences for both individuals and society as a whole, much research has been devoted to this problem. Fetal Alcohol Syndrome provides straightforward facts regarding the impact of alcohol consumption as it affects the development of the embryo and fetus. Surveying current research of fetal alcohol syndrome and its related problems, the book addresses the immediate effects on development at various stages. Long-term action of prenatal alcohol exposure later in life is also considered. A chapter devoted to assessing the behavior of children who were prenatally exposed to alcohol emphasizes the necessity of longitudinal studies of fetal alcohol syndrome. This important reference offers a thorough overview of a problem that cannot be ignored.
This authoritative 1996 publication was the first to review comprehensively the important relationship between maternal alcohol abuse during pregnancy and the resulting in utero damage to the child, and the results of this damage during the development of affected children. It includes important contributions by leading and internationally acclaimed clinicians and researchers. The first part of the book discusses clinical issues of alcohol teratogenicity, the clinical picture of fetal alcohol syndrome, and the epidemiology of maternal alcohol abuse and the developmental outcome of the children. The second part addresses pathogenesis and neuropathology, whilst part three reviews developmental issues in the growing child. The final part evaluates approaches to rehabilitation and intervention, and reviews social and public health issues. This comprehensive account will be of interest to gynaecologists, obstetricians, midwives, neonatologists and paediatricians, and for child and adolescent psychiatrists and psychologists.
Maternal alcohol abuse during pregnancy can result in a range of structural and functional abnormalities that include lifelong physical, mental, behavioral and learning disabilities, now collectively termed as Fetal Alcohol Spectrum Disorders (FASD). The incidence of FASD is now estimated be as high as 10 per 1000 live births. Each year, 40,000 babies are born with FASD in the United States at an estimated cost of $1.4 million per individual and total cost of $6 billion. Because of the magnitude of this problem and because the incidence has not decreased in spite intensive efforts to educate women to not abuse alcohol during pregnancy, ways to prevent or mitigate the effects of prenatal alcohol exposure must be explored in addition to education. Therefore, we wished to identify the precise mechanisms by which alcohol mediates the neurodevelopmental damage in order to develop intervention/amelioration strategies. The present study was conducted using an ovine model system. The large body mass of the ovine fetus, the longer gestation that is more similar to that of humans, and that all three trimester equivalents occur in utero, make the sheep an excellent model to study the effects of alcohol on the developing fetus. Our study establishes that maternal alcohol exposure does not result in fetal cerebral hypoxia. Instead, alcohol results in hypercapnea and acidemia leading to a cascade of events in the maternal and fetal compartments that include deficits in the levels of glutamine and glutamine-related amino acids, alterations in endocrine axes, oxidative stress, alteration in cardiovascular homeostasis and fetal neuronal loss. Further, we demonstrate that inhibiting the novel two-pore domain acid sensitive potassium channel (TASK) expressed in the cerebellar granule cells and the peripheral and central chemoreceptors may prove to a be potential therapeutic strategy. Preventive strategies that are safe to use in pregnant women and that involve glutamine-related pathways are also suggested. Finally, the study also establishes the beneficial effects of moderate alcohol consumption on the fetal skeletal system.
It sounds simple: Women who drink while pregnant may give birth to children with defects, so women should not drink during pregnancy. Yet in the 20 years since it was first described in the medical literature, fetal alcohol syndrome (FAS) has proved to be a stubborn problem, with consequences as serious as those of the more widely publicized "crack babies." This volume discusses FAS and other possibly alcohol-related effects from two broad perspectives: diagnosis and surveillance, and prevention and treatment. In addition, it includes several real-life vignettes of FAS children. The committee examines fundamental concepts for setting diagnostic criteria in general, reviews and updates the diagnostic criteria for FAS and related conditions, and explores current research findings and problems associated with FAS epidemiology and surveillance. In addition, the book describes an integrated multidisciplinary approach to research on the prevention and treatment of FAS. The committee: Discusses levels of preventive intervention. Reviews available data about women and alcohol abuse and treatment among pregnant women. Explores the psychological and behavioral consequences of FAS at different ages. Examines the current state of knowledge about medical and therapeutic interventions, education efforts, and family support programs. This volume will be of special interest to physicians, nurses, mental health practitioners, school and public health officials, policymakers, researchers, educators, and anyone else involved in serving families and children, especially in high risk populations.
These guidelines have been developed to enable professionals to assist women who are pregnant, or have recently had a child, and who use alcohol or drugs or who have a substance use disorder, to achieve healthy outcomes for themselves and their fetus or infant. They have been developed in response to requests from organizations, institutions and individuals for technical guidance on the identification and management of alcohol, and other substance use and substance use disorders in pregnant women. They were developed in tandem with the WHO recommendations for the prevention and management of tobacco use and second-hand smoke exposure in pregnancy.
Alcohol consumption during pregnancy can result in fetal alcohol spectrum disorders (FASD), which encompass a range of physical, behavioral, learning, emotional and social disturbances. Many mechanisms for this array of alcohol-derived fetal injuries have been proposed, but none fully accounts for the deficiencies observed. Alcohol is a ubiquitous drug that may affect the brain at any or all stages of development and at multiple sites; regional differences in vulnerability of different brain structures during different periods of exposure have been demonstrated. This study investigates possible mechanisms for the alcohol induced neurodevelopment damage seen as a result of prenatal alcohol exposure, and also includes evaluation of a potential intervention strategy (glutamine). These experiments all utilized the sheep model, which has distinct advantages over the rodent model for third trimester-equivalent studies (a time of increased vulnerability to the effects of alcohol). The fetal hippocampal formation (pyramidal cells in the CA1 and CA2/3 fields and granule cells of the dentate gyrus) and olfactory bulb (mitral cells) have been altered in response to alcohol exposure in rodent model studies. This study examined the effects on the fetal hippocampal formation and olfactory bulb in response to all three trimester-equivalent alcohol exposure in the sheep model, a species in which the third trimester-equivalent occurs in utero (as opposed to post-natal as occurs in the rodent). It is known that both maternal and fetal cortisol levels increase in response to alcohol. The role of cortisol in mediating fetal cerebellar Purkinje cell loss (known to occur with alcohol exposure) was analyzed. Lastly, the availability of circulating amino acids, both maternal and fetal, in response to alcohol are reported. The results of administration of a single acute dose of glutamine to the ewe, concurrent with alcohol, was evaluated for its ability to prevent the amino acid and pH perturbations known to occur in response to alcohol.