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Fetal environment

Figure 19-1 Classification of placenta shape. Discoid/hemichorial a single placenta is formed, discoid in shape (e.g., primates, rabbits, rodents, humans). Attachment of the primate placenta is bidiscoid and rats and mice have three trophoblastic layers between the maternal and fetal environment. Diffuse/epitheliochorial almost entire surface of the allantochorion is involved in formation of the placenta (e.g., horses, pigs). Zonary/endotheliocorial placenta has complete or incomplete bands of tissue surrounding the fetus (e.g., dogs, cats, seals, bears, and elephants). Cotyledonary multiple discrete areas of attachment called cotyledons are formed by interaction of patches of allantochorion with endometrium. This type of placentation is observed in ruminants. Figure 19-1 Classification of placenta shape. Discoid/hemichorial a single placenta is formed, discoid in shape (e.g., primates, rabbits, rodents, humans). Attachment of the primate placenta is bidiscoid and rats and mice have three trophoblastic layers between the maternal and fetal environment. Diffuse/epitheliochorial almost entire surface of the allantochorion is involved in formation of the placenta (e.g., horses, pigs). Zonary/endotheliocorial placenta has complete or incomplete bands of tissue surrounding the fetus (e.g., dogs, cats, seals, bears, and elephants). Cotyledonary multiple discrete areas of attachment called cotyledons are formed by interaction of patches of allantochorion with endometrium. This type of placentation is observed in ruminants.
There are also issues related to statistical analyses of the data that are unique to behavioral teratology. The offspring of a given litter are not considered as individual subjects since, as members of a litter, they have all experienced factors of the fetal environment which may be unique to their dam. This means that the total number of subjects in a treatment group is really equivalent to the total number of litters represented in that group, a factor which can change the degrees of freedom in the statistical analyses. [Pg.239]

Merlet-Benichou, C. (1999) Influence of fetal environment on kidney development. International Journal of Developmental Biology, 43, 453 156. [Pg.429]

At the present time, the best we can say is that about half the recognized fetal anomalies are caused either solely or partly by impact on the fetal environment. Here partly means the anomaly evidently involves some combination of genetics and environment. I m not concerned in this book with gross malformations of the fetus—the branch of biomedicine called teratology (dysmorphology)—but with changes in prenatal development due to impact on gene expression that can cause... [Pg.20]

Fetal brain development is a vast subject, the focus of hundreds of research laboratories and clinical groups around the world. In this chapter I highlight some of this research to illustrate how the fetal environment can interact with brain development and to identify broadly the points at which that development is most vulnerable to environmental effects that may alter it in some way, whether divergently or disruptively. [Pg.67]

What all these technical details mean for us can be briefly stated in plain English We know enough about the detailed development of the human brain to expect it to be highly vulnerable to impacts on the fetal environment. Neuroscientists are not surprised by correlations between impacts on the fetal environment and later behavior and cognitive performance. The purpose of this chapter has been to explain this lack of surprise. [Pg.84]

The Dutch Hunger Winter, in short, provided one of the major sources of evidence for a new idea in the understanding of later health and disease. This idea forms the hypothetical background for this chapter s focus on specific factors inside and outside the fetal environment that influence, and sometimes disrupt, fetal development. [Pg.86]

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]

The role of the placenta is of critical importance in the development of twins. With identical (monozygotic) twins, even a shared placenta does not guarantee uniformity and equality of the fetal environment.11 Each twin sharing a placenta is supplied by a different portion of the placenta. The sharing is almost always unequal. Delivery of maternal blood differs. The amount of space and the location of each fetus differ. Each twin has a local environment in addition to a general uterine environment. [Pg.93]

Meanwhile, the high prevalence of alcohol use by pregnant women and women of child-bearing age, coupled with the high prevalence of FASD, makes at least one idea seem bizarre the idea that the fetal environment contributes little or nothing to postnatal behavior and IQ. [Pg.141]

Meanwhile, the sexual development of the human fetus is shaped by natural hormonal programming, a consequence of genetics, epigenetics, and a fetal environment that is often malevolent. [Pg.152]

Meanwhile, what needs to be emphasized is that once again both animal and human biology point us to the conclusion that variables in the fetal environment can be important in shaping the behavior of children and adults. [Pg.167]

Cerebral palsy is a salient example of fetal brain injury with many possible causes. I am not making an argument here that every case of cerebral palsy is a result of impacts on the fetal environment only that evidence suggests some cases may indeed have such a cause. Here are some facts10 ... [Pg.174]

The term mental illness is about as ambiguous as you can get, a label that covers everything from mild mood problems to complete derangement in violent paranoid schizophrenia. My focus in this chapter is on those mental disorders for which there is some evidence relating the condition to impacts on the fetal environment. That leaves out many psychiatric conditions known to clinicians, and even many common kinds of mental illness. So the absence of any discussion of some specific mental disorder in this chapter does not mean it s unrelated to the fetal environment—it means only that I know of no sufficient evidence to present here. My purpose here is to show that there s enough scientific and clinical data to suggest there may be important connections between the fetal environment and... [Pg.207]

This section is mostly about schizophrenia because there s intriguing evidence relating the fetal environment to schizophrenia, and not much research yet for most other psychoses. [Pg.211]

FETAL ENVIRONMENT, TEMPERAMENT, AND NONPSYCHOTIC MENTAL ILLNESS... [Pg.223]

Anxiety disorders are a major clinical entity, but there s hardly any unambiguous information yet relating such disorders to the fetal environment, so there s nothing to discuss here. [Pg.224]

Themost common mood disorder in America is major depressive disorder, and we have concrete evidence relating it to the fetal environment—which is why it s discussed here. [Pg.228]

Since we already know that changes in the fetal environment can cause severe changes in the development of the fetal brain and nervous system, one question that pops up is whether mere brain size can explain IQ differences—brain size either determined by genes alone or brain size determined by gene—environment interactions during gestation. [Pg.240]

So differences between people in the sizes of their brains can tell us nothing about the origins of their differences in IQ—and have little relevance for any questions we ask about the fetal environment and intelligence. [Pg.241]

Lower birth weight of an MZ twin compared to the cotwin is associated with lower adult intelligence compared to the cotwin 21 This is a fetal-environment effect that can result from an MZ transfusion syndrome, which occurs only with mono-chorionic MZ twins. The syndrome is a consequence of vascular fusions that cause an unbalanced blood supply between the twins. It is usually fatal for both, but when the twins survive, one twin usually has a lower birth weight. The transfusion syndrome occurs in 5—15 percent of monochorionic MZ pregnancies.22... [Pg.246]

Some have suggested that studies of MZ twins with shared or nonshared chorions are evidence that the fetal environment is not important.25 Since the idea was recently presented in... [Pg.247]

Definitely not. The similar environments in these studies is the postnatal environment. The prenatal environment is never considered in the analysis. For twins reared in similar postnatal environments, we don t know if the higher twin-pair IQ correlations for MZ twins are due to identity of genes or similarity of fetal environments. It is certainly possible that the fetal environments (including reactions to impacts) of identical twins are always more similar than the fetal environments of fraternal twins. We don t know enough yet about human twin biology to discount that possibility. [Pg.249]

In the next chapter I will discuss the impact of socioeconomic factors on the fetal environment. Such factors are not minor, they re numerous, and they vary widely in character and intensity. It s not a surprise that these factors, most prevalent in lower socioeconomic classes, will overshadow any genotype contribution to IQ variance. [Pg.256]

If we re to evaluate the implications of the effects of fetal environment on IQ we need to understand the limitations of the IQ test. The construction of an IQ test involves a normalization process. Items in the test are selected and included so that a sample population will produce a symmetrical bell-shaped distribution of test scores with a mean and median of ioo points and a standard deviation of 15 points. The test is renormalized at intervals of 20 or 25 years to keep the parameters of the distribution curve the same mean and median of 100 points and standard deviation of 15 points. [Pg.256]

In this chapter, I want to give examples of how various cultural factors, in general, and poverty, in particular, impact the fetal environment and through that impact shape later behavior and IQ. [Pg.264]

But no matter the culture, a critical phenomenon needs to be emphasized the impact of culture on the fetal environment, one environment influencing another environment, the fetal environment translating cultural forces into biological effects that shape the development of the brain and nervous system. This connection between culture and brain development is as much anthropology as neuroscience—which makes the connection intriguing and even startling. But more important is that the connection is crucial for public policy. [Pg.266]

Cultural effects are complex, diverse, and not always explicit. In the following sections we consider how geography, maternal behavior, and poverty act as transforming mediators between culture and the fetal environment. What I present here is no more than a meager summary of the available data in the scientific literature the endnotes provide sources to amplify the text. My objective is only to establish a central idea the link between culture and fetal development. [Pg.269]


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See also in sourсe #XX -- [ Pg.20 , Pg.223 , Pg.225 ]




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