Use the template provided below, using the week 2 section for this assignment.
Throughout this course, you will be creating a series of parent handouts focused on the various ages and stages of development. The second week of class has discussed genetic and environmental influences on development, prenatal development, and the newborn stage; therefore, this will be the focus of your Week 2 assignment. Continuing with the same template from your Week 1 Theory Parent Handout assignment, complete the slides for the Week 2 portion.
· Read Chapter 2: Genetic and Environment Foundations
· Review Chapter 3: Prenatal Development
· Review Chapter 4: Birth and the Newborn Baby
· Find and open your latest version of the Parent Handout template on your computer. You will be adding on to this document.
For your assignment, complete the following:
· Describe two genetic factors that can influence prenatal development.
· Describe two environmental factors that can influence prenatal development.
· Discuss how you will use Bronfenbrenner’s ecological systems theory to support families during the prenatal and newborn stage.
· Explain three resources for families to support them during the prenatal and newborn stage of development. Be sure to include a link to each resource.
· One resource should be a quick read for families on the go.
· One resource should be more detailed for families who want to learn more.
· One resource should be user-friendly for diverse families (e.g., ELL, single parents, grandparents raising grandchildren, etc.).
· Explain the role of an educator in supporting the prenatal development of families in their care.
· Describe how the ideas you shared in the parent handout section of this assignment are supported by the theory you aligned with in your Week 1 Discussion: Child Development Theories.
· Discuss how an understanding of each family’s cultural context can make you a more effective educator during this time frame.
The Prenatal and Newborn Parent Handout assignment
· Must be three pages in length and formatted according to template.
· Must utilize academic voice. See the Academic Voice Links to an external site. resource for additional guidance.
· Must use at least two scholarly sources in addition to the course text. These scholarly resources should be different than the resources provided for families. Must follow APA Style Links to an external site. as outlined in the Writing Center.
· The Scholarly, Peer-Reviewed, and Other Credible Sources Links to an external site. table offers additional guidance on appropriate source types. If you have questions about whether a specific source is appropriate for this assignment, please contact your instructor. Your instructor has the final say about the appropriateness of a specific source for a particular assignment.
· To assist you in completing the research required for this assignment, view the Quick and Easy Library Research Links to an external site. tutorial, which introduces the University of Arizona Global Campus Library and the research process, and provides some library search tips.
CHAPTER 2 GENETIC AND ENVIRONMENTAL FOUNDATIONS
Save Our Environment
F. N. Mithila, 12 years, Bangladesh
Children and adults enjoy themselves, embedded in the supportive context of an idyllic urban landscape. Chapter 2 considers how heredity and multiple layers of the surrounding environment jointly influence child development.
Reprinted with permission from The International Museum of Children’s Art, Oslo, Norway
WHAT’S AHEAD IN CHAPTER 2
2.1 Genetic Foundations
The Genetic Code • The Sex Cells • Sex Determination • Multiple Offspring • Patterns of Gene–Gene Interaction • Chromosomal Abnormalities
2.2 Reproductive Choices
Genetic Counseling • Prenatal Diagnosis • Adoption
■ Social Issues: health: The Pros and Cons of Reproductive Technologies
2.3 Environmental Contexts for Development
The Family • Socioeconomic Status and Family Functioning • Affluence • Poverty • Beyond the Family: Neighborhoods and Schools • The Cultural Context
■ Social Issues: education: Worldwide Education of Girls: Transforming Current and Future Generations
■ Cultural Influences: Familism Promotes Competence in Hispanic Children and Youths
2.4 Understanding the Relationship Between Heredity and Environment
The Question, “How Much?” • The Question, “How?”
■ Biology and Environment: The Tutsi Genocide and Epigenetic Transmission of Maternal Stress to Children
It’s a girl!” announces the doctor, holding up the squalling newborn baby as her parents gaze with amazement at their miraculous creation.
“A girl! We’ve named her Sarah!” exclaims the proud father to eager relatives waiting for news of their new family member.
As we join these parents in thinking about how this wondrous being came into existence and imagining her future, we are struck by many questions. How did this baby, equipped with everything necessary for life outside the womb, develop from the union of two tiny cells? What ensures that Sarah will, in due time, roll over, reach for objects, walk, talk, make friends, learn, imagine, and create—just like other typical children born before her? Why is she a girl and not a boy, dark-haired rather than blond, calm and patient rather than energetic and distractible? What difference will it make that Sarah is given a name and place in one family, community, nation, and culture rather than another?
To answer these questions, this chapter takes a close look at the foundations of development: heredity and environment. Because nature has prepared us for survival, all humans have features in common. Yet each of us is also unique. Think about several children you know well, and jot down the most obvious physical and behavioral similarities between them and their parents. Did you find that one child shows combined features of both parents, another resembles just one parent, whereas a third is not like either parent? These directly observable characteristics are called phenotypes. They depend in part on the individual’s genotype—the complex blend of genetic information that determines our species and influences all our unique characteristics. Yet phenotypes are also affected by each person’s lifelong history of experiences.
We begin our discussion with a review of basic genetic principles that help explain similarities and differences among children in appearance and behavior. Then we turn to aspects of the environment that play powerful roles in children’s lives. As our discussion proceeds, some findings may surprise you. For example, many people are convinced that when children inherit unfavorable characteristics, little can be done to help them. Others believe that the damage done to children by a harmful environment can easily be corrected. As we will see, neither of these assumptions is accurate. Rather, heredity and environment continuously collaborate, each modifying—for better or for worse—the power of the other to influence the course of development. ■
2.1 GENETIC FOUNDATIONS
2.1a Explain what genes are and how they are transmitted from one generation to the next.
2.1b Describe various patterns of gene–gene interaction.
2.1c Describe major chromosomal abnormalities, and explain how they occur.
Within each of the trillions of cells in the human body (except red blood cells) is a control center, or nucleus, that contains rodlike structures called chromosomes, which store and transmit genetic information. Human chromosomes come in 23 matching pairs; an exception is the XY pair in males, which we will discuss shortly. Each member of a pair corresponds to the other in size, shape, and genetic functions. One chromosome is inherited from the mother and one from the father (see Figure 2.1 on page 52).
2.1.1 The Genetic Code
Chromosomes are made up of a chemical substance called deoxyribonucleic acid, or DNA. As Figure 2.2 on page 52 shows, DNA is a long, double-stranded molecule that looks like a twisted ladder. Each rung of the ladder consists of a specific pair of chemical substances called bases. It is this sequence of base pairs that provides genetic instructions. Although the bases always pair up in the same way across the ladder rungs—A with T and C with G—they can occur in any order along its sides. A gene is a segment of DNA along the length of the chromosome. Genes can be of different lengths—perhaps 100 to several thousand ladder rungs long. An estimated 19,000 to 20,000 protein-coding genes, which directly affect our body’s characteristics, lie along the human chromosomes (Ezkurdia et al., 2014). They send instructions for making a rich assortment of proteins to the cytoplasm, the area surrounding the cell nucleus. Proteins, which trigger chemical reactions throughout the body, are the biological foundation on which our characteristics are built. An additional 18,000 regulator genes modify the instructions given by protein-coding genes, greatly complicating their genetic impact (Pennisi, 2012).
Figure 2.1 A karyotype, or photograph, of human chromosomes. The 46 chromosomes shown on the left were isolated from a human cell, stained, greatly magnified, and arranged in pairs according to decreasing size of the upper “arm” of each chromosome. The twenty-third pair, XY, reveals that the cell donor is a genetic male. In a genetic female, this pair would be XX.
© CNRI/SCIENCE SOURCE
We share some of our DNA with even the simplest organisms, such as bacteria and molds, and most of it with other mammals, especially primates. About 99 percent of chimpanzee and human DNA is identical. And the genetic variation from one human to the next is even less: Individuals around the world are about 99.6 percent genetically identical (Tishkoff & Kidd, 2004; Wong, 2014). But these straightforward comparisons are misleading. Many human DNA segments that appear like those of chimpanzees have undergone duplications and rearrangements with other segments. So in actuality, the species-specific genetic material responsible for the attributes that make us human, from our upright gait to our extraordinary language and cognitive capacities, is extensive (Sudmant et al., 2015). Furthermore, it takes a change in only a single DNA base pair to influence human traits. And such tiny changes generally combine in unique ways across multiple genes, amplifying human variability.
Figure 2.2 DNA’s ladderlike structure. A gene is a segment of DNA along the length of the chromosome, varying from perhaps 100 to several thousand ladder rungs long. The pairings of bases across the rungs of the ladder are very specific: Adenine (A) always appears with thymine (T), and cytosine (C) always appears with guanine (G).
How do humans, with far fewer genes than scientists once thought, manage to develop into such complex beings? The answer lies in the proteins our genes make, which break up and reassemble in staggering variety—about 10 to 20 million altogether. Simpler species have far fewer proteins. Furthermore, the communication system between the cell nucleus and cytoplasm, which fine-tunes gene activity, is more intricate in humans than in simpler organisms. Finally, within the cell, environmental factors modify gene expression. Many such effects are unique to humans and influence brain development (Lussier, Islam, & Kobor, 2018). So even at this microscopic level, biological events of profound developmental significance are the result of both genetic and nongenetic forces.
2.1.2 The Sex Cells
New individuals are created when two special cells called gametes, or sex cells—the sperm and ovum—combine. A gamete contains only 23 chromosomes, half as many as a regular body cell. Gametes are formed through a cell division process called meiosis, which halves the number of chromosomes normally present in body cells. When sperm and ovum unite at conception, the resulting cell, called a zygote, will again have 46 chromosomes. Meiosis ensures that a constant quantity of genetic material is transmitted from one generation to the next.
In meiosis, the chromosomes pair up and exchange segments, so that genes from one are replaced by genes from another. This shuffling of genes creates new hereditary combinations. Then chance determines which member of each pair will gather with others and end up in the same gamete. These events make the likelihood that nontwin siblings will be genetically identical about 1 in 700 trillion, or virtually nil. The genetic variability produced by meiosis is adaptive: It increases the chances that at least some members of a species will cope with ever-changing environments and will survive.
In the male, the cells from which sperm arise are produced continuously throughout life, so a healthy man can father a child at any age after sexual maturity. The female is born with a bank of ova already present in her ovaries, though recent findings suggest that new ova may arise from ovarian stem cells later on (Virant-Klun, 2015). Still, there are plenty of female sex cells. About 1 to 2 million are present at birth, 40,000 remain at adolescence, and approximately 350 to 450 female sex cells will mature during a woman’s childbearing years (Moore, Persaud, & Torchia, 2016).
2.1.3 Sex Determination
Return to Figure 2.1 and note that 22 of the 23 pairs of chromosomes are matching pairs, called autosomes (meaning not sex chromosomes). The twenty-third pair consists of sex chromosomes. In females, this pair is called XX; in males, it is called XY. The X is a relatively long chromosome, whereas the Y is short and carries little genetic material. When gametes form in males, the X and Y chromosomes separate into different sperm cells. The gametes that form in females all carry an X chromosome. Therefore, the genetic sex of the new organism is determined by whether an X-bearing or a Y-bearing sperm fertilizes the ovum. In fact, scientists have isolated a gene on the Y chromosome that initiates the formation of male sex organs during the prenatal period (Sekido & Lovell-Badge, 2009). Additional genes, some yet to be identified, are involved in the development of sexual characteristics.
Biologists caution that human sexual diversity is much wider than a simple male–female dichotomy. As a result of variations in genes or chance events in development, some individuals’ sex chromosomes do not match their sexual anatomy. An estimated 1 in every 100 people are affected, usually mildly but occasionally substantially (Ainsworth, 2015). The existence of people with intersex traits, many of whom go through life unaware of their condition unless they seek treatment for infertility or another medical issue, is redefining sex as a spectrum.
2.1.4 Multiple Offspring
Ruth and Peter, a couple I know well, tried for several years to have a child, without success. Eventually, Ruth’s doctor prescribed a fertility drug, and twins—Jeannie and Jason—were born. Jeannie and Jason are fraternal, or dizygotic, twins, the most common type of multiple offspring, resulting from the release and fertilization of two ova. Genetically, they are no more alike than ordinary siblings. Table 2.1 on page 254 summarizes genetic and environmental factors that increase the chances of giving birth to fraternal twins. Older maternal age, fertility drugs, and in vitro fertilization are major causes of the dramatic rise in fraternal twinning and other multiple births in industrialized nations over the past several decades. Currently, fraternal twins account for 1 in about every 33 births in the United States (Martin et al., 2017).
Table 2.1 Maternal Factors Linked to Fraternal Twinning
Occurs more often among women whose families contain fraternal twins, suggesting a genetic influence. Two recently identified genes, one that augments hormone levels and another that may heighten the ovaries’ responsiveness to hormones, increase the chances of fraternal twinning.
Occurs in 6 per 1,000 births in Asia and Latin America, 9 to 12 per 1,000 births in White Europeans, and 40 per 1,000 births among Black Africansa
Rises with maternal age, peaking between 35 and 39 years, and then rapidly falls
Occurs more often among women who are tall and overweight or of normal weight as opposed to slight body build
Number of births
Is more likely with each additional birth
Fertility drugs and in vitro fertilization
Is more likely with fertility hormones and in vitro fertilization (see page 61), which also increase the chances of bearing higher-order multiples
a Worldwide rates, not including multiple births resulting from use of fertility drugs.
Sources: Hoekstra et al., 2008, 2010; Kulkarni et al., 2013; Smits & Monden, 2011; Mbarek et al., 2016.
Twins can also be created when a zygote that has started to duplicate separates into two clusters of cells that develop into two individuals. These are called identical, or monozygotic, twins because they have the same genetic makeup. The frequency of identical twins is the same around the world—about 3 to 4 per 1,000 births (Kulkarni et al., 2013). Animal research has uncovered environmental influences that prompt this type of twinning, including temperature changes, variation in oxygen levels, and late fertilization of the ovum (Lashley, 2007). In a minority of cases, identical twinning runs in families, but this occurs so rarely that it is likely due to chance rather than heredity.
During their early years, children of single births often are healthier and develop more rapidly than twins. Jeannie and Jason, like most twins, were born several weeks prematurely and required special care in the hospital. When the twins came home, Ruth and Peter had to divide time between them. Perhaps because neither baby received as much attention as the average single infant, Jeannie and Jason walked and talked several months later than most children their age, though like most twins they caught up in development by middle childhood (Lytton & Gallagher, 2002; Nan et al., 2013; Raz et al., 2016). Parental energies are further strained after the birth of triplets, whose early development is slower than that of twins (Feldman, Eidelman, & Rotenberg, 2004).
These identical, or monozygotic, twins were created when a duplicating zygote separated into two clusters of cells, which developed into two individuals with the same genetic makeup.
© RAY EVANS/ALAMY STOCK PHOTO
2.1.5 Patterns of Gene–Gene Interaction
Jeannie has her parents’ dark, straight hair; Jason is curly-haired and blond. The way genes from each parent interact helps explain these outcomes. Recall that except for the XY pair in males, all chromosomes come in matching pairs. Two forms of each gene occur at the same place on the chromosomes, one inherited from the mother and one from the father. Each form of a gene is called an allele. If the alleles from both parents are alike, the child is homozygous and will display the inherited trait. If the alleles differ, then the child is heterozygous, and relationships between the alleles influence the phenotype.
In many heterozygous pairings, dominant–recessive inheritance occurs: Only one allele affects the child’s characteristics. It is called dominant; the second allele, which has no effect, is called recessive. Hair color is an example. The allele for dark hair is dominant (we can represent it with a capital D), whereas the one for blond hair is recessive (symbolized by a lowercase b). Both a child who inherits a homozygous pair of dominant alleles (DD) and a child who inherits a heterozygous pair (Db) will be dark-haired, even though their genotypes differ. Blond hair (like Jason’s) can result only from having two recessive alleles (bb). Still, heterozygous individuals with just one recessive allele (Db) can pass that trait to their children. Therefore, they are called carriers of the trait.
Most recessive alleles—like those for blond hair, pattern baldness, or nearsightedness—are of little developmental importance. But some cause serious disabilities and diseases. One well-known recessive disorder is phenylketonuria, or PKU, which affects the way the body breaks down proteins contained in many foods. Infants born with two recessive alleles lack an enzyme that converts one of the basic amino acids that make up proteins (phenylalanine) into a byproduct essential for body functioning (tyrosine). Without this enzyme, phenylalanine quickly builds to toxic levels that damage the central nervous system, causing permanent intellectual disability.
Despite its potentially damaging effects, PKU illustrates that inheriting unfavorable genes does not always lead to an untreatable condition. All U.S. states require that each newborn be given a blood test for PKU. If the disease is found, doctors place the baby on a diet low in phenylalanine. Children who receive this treatment nevertheless show mild deficits in control of attention, memory, planning, decision making, and problem solving, because even small amounts of phenylalanine interfere with brain functioning (Fonnesbeck et al., 2013; Jahja et al. 2014). But as long as dietary treatment begins early and continues, children with PKU usually attain an average level of intelligence and have a normal lifespan.
In dominant–recessive inheritance, if we know the genetic makeup of the parents, we can predict the percentage of children in a family who are likely to display or carry a trait. Figure 2.3 illustrates this for PKU. For a child to inherit the condition, each parent must have a recessive allele. But because of the action of regulator genes, children vary in the degree to which phenylalanine accumulates in their tissues and in the extent to which they respond to treatment.
Figure 2.3 Dominant–recessive mode of inheritance, as illustrated by PKU. When both parents are heterozygous carriers of the recessive gene (p), we can predict that 25 percent of their offspring are likely to be normal (NN), 50 percent are likely to be carriers (Np), and 25 percent are likely to inherit the disorder (pp). Notice that the child with PKU, in contrast to his siblings, has light hair. The recessive gene for PKU affects more than one trait. It also leads to fair coloring.
Only rarely are serious diseases due to dominant alleles. Think about why this is so. Children who inherit the dominant allele always develop the disorder. They seldom live long enough to reproduce, so the harmful dominant allele is eliminated from the family’s heredity in a single generation. Some dominant disorders, however, do persist. One is Huntington disease, a condition in which the central nervous system degenerates. Its symptoms usually do not appear until age 35 or later, after the person may have passed the dominant allele to his or her children.
In some heterozygous circumstances, the dominant–recessive relationship does not hold completely. Instead, we see incomplete dominance, a pattern of inheritance in which both alleles are expressed in the phenotype, resulting in a combined trait, or one that is intermediate between the two.
The sickle cell trait, a heterozygous condition present in many Black Africans, provides an example. Sickle cell anemia occurs in full form when a child inherits two recessive alleles. They cause the usually round red blood cells to become sickle (crescent-moon) shaped, especially under low-oxygen conditions. The sickled cells clog the blood vessels and block the flow of blood, causing intense pain, swelling, and tissue damage. Despite medical advances that today allow 85 percent of affected children to survive to adulthood, North Americans with sickle cell anemia have an average life expectancy of only 55 years (Chakravorty & Williams, 2015). Heterozygous individuals are protected from the disease under most circumstances. However, when they experience oxygen deprivation—for example, at high altitudes or after intense physical exercise—the single recessive allele asserts itself, and a temporary, mild form of the illness occurs.
The sickle cell allele is common among Black Africans for a special reason. Carriers of it are more resistant to malaria than are individuals with two alleles for normal red blood cells. In Africa, where malaria is common, these carriers survived and reproduced more frequently than others, leading the gene to be maintained in the Black population. But in regions of the world where the risk of malaria is low, the frequency of the gene is declining. For example, only 8 percent of African Americans are carriers, compared with 20 percent of Black Africans (Centers for Disease Control and Prevention, 2017h).
Males and females have an equal chance of inheriting recessive disorders carried on the autosomes. When a harmful allele is carried on the X chromosome, however, X-linked inheritance applies, making males more likely to be affected because their sex chromosomes do not match. In females, any recessive allele on one X chromosome has a good chance of being suppressed by a dominant allele on the other X. But the Y chromosome is only about one-third as long and therefore lacks many corresponding alleles to override those on the X.
A well-known example of X-linked inheritance is hemophilia, a disorder in which the blood fails to clot normally. Figure 2.4 shows its greater likelihood of inheritance by male children whose mothers carry the abnormal allele. Another example is fragile X syndrome, the most common inherited cause of intellectual disability. In this disorder, which affects about 1 in 2,000 males and 1 in 6,000 females, an abnormal repetition of a sequence of DNA bases occurs on the X chromosome, damaging a particular gene. In addition to cognitive impairments, the majority of individuals with fragile X syndrome suffer from attention deficits and high anxiety, and about 30 to 35 percent also have symptoms of autism (Wadell, Hagerman, & Hessl, 2013). Because the disorder is X-linked, males are more often affected.
Besides X-linked disorders, many sex differences reveal the male to be at a disadvantage. Rates of miscarriage, infant and childhood deaths, birth defects, learning disabilities, behavior disorders, and intellectual disability all are higher for boys (Boyle et al., 2011; MacDorman & Gregory, 2015). It is possible that these sex differences can be traced to the genetic code. The female, with two X chromosomes, benefits from a greater variety of genes. Nature, however, seems to have adjusted for the male’s disadvantage. Worldwide, about 103 boys are born for every 100 girls, and an even greater number of males are conceived (United Nations, 2017).
In cultures with strong gender-biased attitudes that induce expectant parents to prefer a male child, the male-to-female birth sex ratio is often much larger. In China, for example, the spread of ultrasound technology (which enables prenatal sex determination) and enforcement of a one-child family policy to control population growth—both of which began in the 1980s—led to a dramatic increase in sex-selective abortion. In 2015, China ended its one-child policy, substituting a two-child policy. Nevertheless, many Chinese couples continue to say they desire just one child (Basten & Jiang, 2015; Jiang, Li, & Sanchez-Barricarte, 2016). Today, China’s birth sex ratio is 117 boys for every 100 girls—a gender imbalance with adverse social consequences, such as rising crime rates and male competition for marriage partners.
Figure 2.4 X-linked inheritance. In the example shown here, the allele on the father’s X chromosome is normal. The mother has one normal and one abnormal recessive allele on her X chromosomes. By looking at the possible combinations of the parents’ alleles, we can pr
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