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Fetal environmental impact

And this is very relevant for the way we think about fetal development. The more complex the process that reads out genetic information stored in the genome, the more complex is the vulnerability of that process to environmental impact. [Pg.47]

We know that in the mature brain, neurotransmitters are released by nerve cell endings and act at synapses to mediate the interaction between nerve cells. There s now evidence that during the development of the prenatal brain, neurons can release transmitters before any connections are made, and that such released transmitters, acting as trophic factors, guide the formation of connections.17 Any environmental impact or mutation that affects the synthesis or release of neurotransmitters can be expected to have an effect on the development of the fetal brain. For example, during fetal development in Down syndrome, reductions apparently occur in the levels of various neurotransmitters. This may be one mechanism for the impaired brain development characteristic of this syndrome.18... [Pg.82]

In this book I use the term fetal programming —without reference to mechanism—to describe environmental impact of any kind on the fetus that produces alterations in health and disease apparent at any time in childhood or adulthood. This idea is essentially an extension into the prenatal period of more general conclusions about the role of early experience in later life. Included in this conception are postnatal temperament, behavior patterns, intelligence, psychopathology, and so on—the behavioral focus of this book. The point is that sometimes postnatal consequences of prenatal environmental impacts involve more than just alterations in the physiology of organ systems—such impacts can also have consequences for later behavior and cognitive performance. [Pg.88]

During fetal development, there are critical periods of vulnerability to environmental impacts, the critical periods occurring at various times in different tissues. Cells rapidly dividing to form tissues and organs are at greatest risk, and it s reasonable that fetal programming is more likely to occur in such tissues. [Pg.88]

The most important general idea about the fetal environment is that any impact that results in physiological stress for the fetus can be a risk factor for adverse developmental and health outcomes. This is clear only from animal experiments. For humans, on whom comparable experiments are not possible, we must depend on empirical data, on correlations, and on deductions. Moreover, because the physiology, chemistry, hormone profile, and so on of the embryo and fetus are continually changing during gestation, the developmental consequences of an environmental impact depend on when it occurs, and on its duration, severity, and type. [Pg.92]

Prenatal development is subject to a variety of environmental impacts that can divert, disrupt, and stop development altogether. The effects may not be observable at birth, but many of them affect later cognitive performance and emotional stability that may remain subclinical and may never be considered as deriving from the fetal period. [Pg.121]

Not quite. Autism in identical twins can be caused by a shared fetal environmental impact rather than by direct genetic transmission. The reality is that like mental retardation, autism is a behaviorally defined syndrome with a possibly wide variety of both genetic and nongenetic causes. The often-quoted concordance rate of 90 percent among identical twins is accurate for broad autism but not for severe (narrow) autism, for which twin concordance is only about 60 percent. Also in contrast to the ABC News report, the concordance among fraternal twins can be as high as 23 percent for broad autism.55... [Pg.194]

Meanwhile, what is needed is an understanding of neurological and psychiatric realities. Every fetal environmental impact discussed in this book that we know produces changes in the developing brain and consequent cognitive and emotional deficits has the potential to be related to childhood and adult violence and criminal behavior. [Pg.299]

Recently, Harrison and Sharp and Irvine summarized the hypothesis and status of evidence implicating endocrine disruption and their adverse impacts on human health (Sharp and Skakkebaek, 1993 Harrison, 2001 Sharp and Irvine, 2004). They outlined that exposure of the fetal/ developing male to environmental pollutants resulted in hypospadias, cryptorchidism, prostrate cancer, testicular cancer, a global decrease in sperm counts, and decreased male reproductive capacity. Detrimental effects in women include breast cancer, cystic ovaries, and endometriosis. [Pg.733]

I look at many possible causes of fetal damage in this book, but give particular emphasis to man-made environmental toxins, be they chemical pollutants in our air, water, and land, or substances in the consumer marketplace, legal and otherwise. The effects of these toxins are often connected to more than one type of fetal damage. Prenatal exposure to lead, for example, is connected to postnatal occurrences of lower IQ, ADHD, and schizophrenia, usually in different individuals. Prenatal exposure to tobacco smoke, as another example, is connected to a host of effects with adverse postnatal consequences as well. The effects of both sorts of toxins can also be related to other fetal impacts, which in turn are often connected to important social... [Pg.21]

The major problem concerning the impact of environmental neurotoxins on fetal brain development is not the absence of evidence but the absence of research on the many new chemicals in our midst. Regardless, the evidence that we do have tells us that simplistic genetic-determinist arguments about IQ are dubious. [Pg.243]

The factors are diverse, ranging from caffeine consumption during pregnancy to maternal age at conception. The environmental agents with potential adverse impacts on fetal development for which there is the strongest evidence are all culture-dependent tobacco smoke, alcohol (ethanol), cocaine, and combustion-engine carbon monoxide.4 In this book I focus only on factors for which there is evidence known to me. What the factors all have in common is that all have heavy cultural... [Pg.265]


See other pages where Fetal environmental impact is mentioned: [Pg.74]    [Pg.96]    [Pg.122]    [Pg.194]    [Pg.195]    [Pg.272]    [Pg.357]    [Pg.128]    [Pg.4]    [Pg.55]    [Pg.170]    [Pg.384]    [Pg.541]    [Pg.436]    [Pg.77]    [Pg.120]    [Pg.499]    [Pg.261]    [Pg.224]    [Pg.608]   
See also in sourсe #XX -- [ Pg.194 , Pg.299 ]




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