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Genetic Terminology
● Heredity : the passing on of traits from parents to their offspring
● Genes : section of chromosomes that code for traits
● Allele : two or more different versions of a gene (ex. Brown vs. Green iris)
● Genome : the complete set of genes of any organism
● Chromosome : molecules of DNA that transmit genetic information
● DNA : molecules that carry all the biochemical instruction s involved in the formation
and functions of an organism
● Genotype : the genetic material that an individual inherits
● Phenotype : the observable expression of the genotype, including both physical
characteristics and behaviour
● Environment : every experience to which an individual is exposed in their
surroundings; everything other than genes
Genetics Overview
Every cell contains chromosomes which are composed of DNA
● DNA – long chain or double helix of molecules containing the instructions for building
and maintaining the organism
● Chromosome – molecules of DNA that transmit genetic information – in humans
there are 23 pairs of chromosomes (46 total)
Genes are section of chromosomes, each containing instructions for making proteins and giving
rise to specific traits:
● Physical traits (eye color, hair type, height)
● Psychological traits (aggression, anxiety)
Genes are the basic unit of heredity in all living things
● Heredity = passing on traits from parents to offspring
The Genome :
● A complete set of genes found in a particular organism
● Humans' genes are 99.9% the same as any other human
● You genes are also:
○ 96% the same as a chimpanzee
○ 90% the same as a cat
○ 80% the same as a cow
○ 60% he same as a banana
Nature-Nurture Interactions
Genotypes vs. Phenotypes
Genotype: Phenotype:
Genetic material an individual inherits how the genotype is expressed in body and
behaviour
Parent's genotype --> child's genotype
Parent's Genotype --> Child's Genotype
How a child develops is a function of genetic and environmental factors = Nature + nurture
● Children inherit their genotype from their parents
○ One chromosome in each pair from each parent
● What explains all the variability in humans?
○ Independent (random) Assortment of chromosomes
■ Sperm/ovum each have 23 chromosomes
■ When united, they form 23 pairs
○ Crossing over: pairs of chromosomes swap sections of DNA during the
creation of gametes
● Results in gametes with a unique mix of genetic material, different from the original
chromosomes they came from
Child's Genotype --> Child's Phenotype
How a child develops is a function of genetic and environmental factors
● Not all genetic material will be expressed
● Genes often have two or more different forms known as alleles
● Alleles can be dominant or recessive
○ Dominant alleles: always expressed over other alleles
○ Recessive alleles: only expressed in the absence of dominant alleles
● Only a small percent of DNA (~1%) codes for the proteins
● Regulator genes switch other genes "on" and "off":
○ If a gene never gets "switched on", it will not be expressed and will not be
expressed in the phenotype
○ Continuously switching genes on and off at the right time guides
development, prenatally and beyond
● Environmental factors influence regulator genes:
○ Ex. Prenatal exposure to thalidomide
■ Throws off regulator genes during sensitive period of limb
development
■ Genes were there, but just did not get turned on
● While some phenotypes (ex. Blood type) are determined by single genes, most
genes are polygenic
○ Polygenic: determined by more than one gene
Environment --> Child's Phenotype
○ Greater similarity in related than unrelated folks
● Look at degree of relatedness as well :
○ If a trait has a genetic component, siblings should be more alike than
cousins
○ Family members should be more alike than non-family members
○ Families also environment
Investigating Hereditary
Twin Studies
● Look to see how much identical vs. Fraternal twins resemble each other on a specific
trait
Identical Twins (Monozygotic)
● Occurs when a zygote (ball of fertilized cells) splits early in prenatal development
● Close to 100% shared genotype
● Whether monozygotic twins share a placenta and/or amniotic sac depends on when
the zygote divides:
● Divides before implantation: each has a placenta/sac
● Divides early after implantation: shared placenta, independent sacs
● Divides later after implantation: shared placenta and sac
Fraternal Twins (Dizygotic)
● Occurs when two ova are fertilized by two different sperm cells (two separate
organisms)
● Average 50% shared genotype – same as any other sibling
● Share aspects of prenatal environment too, while regular siblings do not
Twin studies
● Assumption: all twins share similar environments so differences must be due to
differing genotypes
○ Identical twins come from the same egg and share the same genes
○ Fraternal twins come from 2 different eggs so they share the same
amount of DNA as 2 regular siblings
● Scientists look at how similar twins are:
○ If identical twins are more alike than fraternal twins, it suggests that genes
play a big role
○ If identical and fraternal twins are equally similar, it suggests environment
may matter more
● The issue:
○ Identical twins might not just share genes – they may also get similar
treatment from family, teachers, friends (environment)
○ Even before birth, their prenatal environment (womb) is often more alike
than fraternal twins'
○ Therefore, twin studies are helpful but not perfect because it is hard to tell
whether similarities come from genes, the environment, or both
● Why do we care whether twins share a placenta/amniotic sac?
○ It gives us insight into the influence of the prenatal environment
○ The greater the similarity between twins sharing a placenta = bigger
influence of the prenatal environment on outcomes
Adoption studies:
● Look to see how much adopted children resemble their biological vs their adoptive
parents
○ If there is a greater similarity to the biological parents --> there must be a
stronger influence of the genotype
○ If there is a greater similarity to the adoptive parents --> there must be a
stronger influence of the environment
● Overall, even though nature and nurture are both always in play, it is the degree that
heredity is involved that is the real question.
Brain Development
Major Processes in Brain Development:
● Neurogenesis: proliferation (rapid increase) of neurons through cell division; begins
weeks after conception
○ After creation, these neurons migrate to their ultimate location
○ They grow and differentiate according to their role
● Synaptogenesis: the formation of synapses with other neurons, making trillions of
connections
○ Too many connections are formed!!
● Synaptic Pruning: process by which synapses that are rarely activated are eliminated
○ Only the useful pathways are preserved
○ Timeline of pruning varies by region
Plasticity – Capacity for the brain to be changed by experience
● Experience-expectant plasticity:
● F rontal = Future planning
● P arietal = Position in space
● T emporal = Talking & Tunes
● O ccipital = Optics (vision)
Over the life span, the density of synapses in a particular cortical area continues to increase
sharply after birth and shows some level of decrease with age
Epigenetics studies the stable changes in gene expressions that are mediated by the
environment
Nature and Nurture Long before there was any understanding of the principles of heredity, people were aware that some characteristics “run in families” and that this tendency was somehow related to procreation. Our modern understanding of how characteristics are transmitted from parent to offspring originated with Gregor Mendel, a nineteenth-century Austrian monk who observed distinct patterns of inheritance in cross-bred pea plants. A much deeper understanding came in the 1950s with James Watson, Francis Crick, and Rosalind Franklin’s identification of the structure of DNA, the basic component of hereditary transmission.
In recent decades, we have seen enormous progress in deciphering the genetic code. Researchers have mapped the entire genome—the complete set of an organism’s genes—of myriad species of plants and animals, including humans. As of 2023, the Genome Variation Map included the complete genomes of 40 species (Li, Putallaz, & Su, 2021). (Visit the Genome Variation Map website if you are curious!) Along with innovations in gene sequencing have come innovations in gene synthesis, a method for producing DNA. While gene synthesis holds significant potential for scientific and medical advances, it is also fraught with ethical concerns. Indeed, the November 2018 announcement by a Chinese scientist about the first genome-edited newborns—twins, one of whose genes was edited to resist HIV—was met with widespread outrage in the scientific community. Critics have raised concerns about the unintended consequences such manipulation might hold for brain function and behaviour not just of these individuals, but of any progeny that also inherits the new genes (Cohen, 2018). Comparisons of the genomes of various species have revealed numerous surprises. One was the number of genes that humans have: our roughly 20,000 to 21,000 protein-coding genes (Willyard, 2018) is far fewer than previous estimates, which ranged from 35,000 to more than 100,000 genes (Ezkurdia et al., 2014). A second surprise was that most of those genes are possessed by all living things. Most human genes are devoted, in decreasing order, to making us animals, vertebrates, mammals, primates, and—finally—humans. A third surprise is that genes themselves make up only about 1% of the human genome. Much of the rest of our genome is made up of noncoding DNA—once thought to be “junk” DNA—that plays a crucial role in regulating the activity of protein-coding genes. Genetic and Environmental Forces To simplify our discussion of the complex interactions amongst genetic and environmental factors, we will organize it around the model shown in Figure 3.1. Three key elements are the genotype, which is inherited genetic material; the phenotype, the observable expression of the genotype, including both body characteristics and behaviour; and the environment, which incorporates every aspect of individuals and their surroundings (including prenatal experience) other than the genes themselves.
These three elements are involved in five relations that are fundamental in the development of every child: (1) parents’ genetic contribution to children’s genotypes; (2) the contribution of children’s genotypes to their own phenotypes; (3) the contribution of children’s environments to their phenotypes; (4) the influence of children’s phenotypes on their environments; and (5) the influence of children’s environments on their genotypes. We will consider each of these relations in turn.
1 Parents’ Genotype–Child’s Genotype Relation 1 involves the transmission of genetic material from parent to offspring. You caught a glimpse of this process in Chapter 2, when we discussed the gametes (one from each biological parent) that conjoin to create a zygote. The nucleus of every cell in the body contains chromosomes, long threadlike molecules made up of two twisted strands of DNA (deoxyribonucleic acid). DNA carries all the biochemical instructions involved in the formation and functioning of an organism. These instructions are “packaged” in genes, the basic unit of heredity in all living things. Each gene is a segment of DNA that is the code for the production of particular proteins. Some proteins are the building blocks of the body’s cells; others regulate the cells’ functioning. Genes affect development and behaviour only through the manufacture of proteins. Human heredity Humans have a total of 46 chromosomes, divided into 23 pairs, in the nucleus of each cell (see Figure 3.2). Each chromosome pair carries, usually at corresponding locations, genes of the same type—that is, sequences of DNA that are relevant to the same traits. Because each parent passes along one chromosome to their offspring, every individual has two copies of each gene.
Genetic diversity and individual differences Genes guarantee that humans will be similar to one another in certain ways, both at the species level (e.g., humans are bipedal and have opposable thumbs) and at the individual level (i.e., family resemblances). Genes also guarantee differences at both levels. Several mechanisms contribute to genetic diversity amongst people. One mechanism that promotes variability amongst individuals is the random assortment of chromosomes in the formation of egg and sperm. During gamete division, the 23 pairs of
chromosomes are shuffled randomly, with chance determining which member of each pair goes into each new egg or sperm. When a sperm and an egg unite, the odds are essentially zero that any two individuals—even members of the same family—will have the same genotype (except, of course, identical twins). Further variation is introduced by a process called crossing over: when gametes divide, the two members of a pair of chromosomes sometimes swap sections of DNA. As a result, some of the chromosomes that parents pass on to their offspring are constituted differently from their own. A second mechanism that enhances variability is mutation, a change in a section of DNA. Some mutations are random, spontaneous errors; others are caused by environmental factors. Those that occur in gametes (germ cells) can be passed on to offspring. Many inherited disorders originate from a mutated gene, as discussed in Box 3.2 in the next section. Most mutations are harmful. Occasionally, however, a mutation enhances the individual’s genetic fitness by increasing disease resistance or allowing the individual to adapt to some crucial aspect of the environment. Such mutations provide the basis for evolution: individuals with the favourable mutated gene are more likely to survive long enough to produce offspring, who, in turn, are likely to possess the mutated gene, thus heightening their own chance of surviving and reproducing. Across generations, these favourable genes proliferate in the gene pool of the species. Children inherit half of their genes from each biological parent. But mechanisms like random assortment and crossing over, as well as forces influencing the child’s phenotype, shape the degree to which a child will resemble one parent and the degree to which they will vary. In the case of the British royals pictured here, Prince George (right) bears a strong resemblance to his father, Prince William (left) at age 2. Sex determination The sex chromosomes are an exception to the general pattern of chromosome pairs just described. Most people who are assigned female at birth have two identical, largish sex chromosomes called X chromosomes, and most people who are assigned male at birth have one X chromosome and one much smaller Y-shaped chromosome. Because genetically female people have only X chromosomes, the division of their germ cells results in all their eggs having an X. However, because genetically male people have XY chromosomal pairs, half of their sperm contain an X chromosome and half contain a Y. For this reason, the genetically male parent always determines the genetic sex of offspring. If an X-bearing sperm fertilizes an egg, a female (XX) zygote results; if a Y-bearing sperm fertilizes an egg, a male (XY) zygote results. A gene on the Y chromosome encodes the protein that triggers the prenatal formation of testes by activating genes on other chromosomes, triggering the production of the hormone testosterone (as discussed in Chapter 2). It should be noted that sex chromosomes are one of several primary and secondary characteristics in the spectrum of biological sexual variation, and that sex, referring to this biological spectrum, is distinct from gender, which refers to social and cultural attributes associated with a person’s identity. Sexual and gender development are discussed in detail in Chapter 15. 2 Child’s Genotype–Child’s Phenotype We now turn to Relation 2 in Figure 3.1, the relation between one’s genotype and one’s phenotype. Keep in mind that phenotypes include both physical characteristics, such as height and eye colour, and behavioural characteristics, such as temperament and intelligence. Genes also influence unobservable, intermediate aspects of the phenotype that impact behaviour, most notably, our brain and nervous systems. These intermediate phenotypes, known as endophenotypes, mediate the pathways between genes and behaviour. Although every cell in your body contains copies of all the genes you received from your parents, only some of those genes are expressed. At any given time in any cell in the body, some genes are active (turned on), while others are not. Some genes that are hard at work in neurons, for example, are totally at rest in toenail cells. Gene expression: Developmental changes From conception to death, genes influence an individual’s development and behaviour only if they are switched on and off in the right place, at the right time, and for the right length of time. Some genes are turned on in only a few cells and for only a few hours and then are switched off permanently. This pattern is typical during embryological development when, for instance, the genes that are turned on in certain cells lead them to specialize for arm, hand, and fingerprint formation. Other genes are involved in the basic functioning of almost all cells almost all the time. The switching on and off of genes is controlled primarily by regulator genes. The activation or inactivation of one gene is always part of a chain of genetic events. When one gene is switched on, it causes another gene to turn on or off, which has an impact on the status of yet other genes. Thus, genes never function in isolation. Rather, they belong to extensive networks in which the expression of one gene is a precondition for the expression of another, and so on. The fact that regulator genes can repeatedly switch other genes on and off in different patterns means that a given gene can function multiple times in multiple places during development. This on-again, off-again functioning of individual genes results in enormous diversity in genetic expression. By analogy, consider the fact that this book is written with only 26 letters, and probably only a few thousand different words made up of combinations of those letters. The meaning comes from the order in which the letters have been “switched on and off” by the authors. External factors also affect the switching on and off of genes. A dramatic example is the effect of thalidomide on limb development (described in Chapter 2), in which the sedative interferes with the functioning of genes underpinning normal growth factors. Another example relates to vision. Early visual experience is necessary for the normal development of the visual system because it causes the switching on of certain genes, which, in turn, switch on other genes in the visual cortex (Maya-Vetencourt & Origlia, 2012). The ramifications of decreased visual experience are observed in cases of children with cataracts that are not removed early in life, as discussed later in this chapter. Gene expression: Dominance patterns Many of an individual’s genes are never expressed; some others are only partially expressed. What factor determines whether a gene is expressed? One-third of human genes have two or more different forms, known as alleles. The alleles of a given gene influence the same trait or characteristic (e.g., eye colour), but they contribute to different developmental outcomes (e.g., brown, blue, hazel, grey eyes). Perhaps the simplest pattern of gene expression—discovered by Mendel—is referred to as the dominant–recessive pattern. Some genes have only two alleles, one of which is dominant and the other recessive. In this pattern, there are two possibilities: (1) a person can inherit two of the same allele—two dominant or two recessive—and thus be homozygous for the trait in question; or (2) the person can inherit two different alleles—one dominant and the other recessive—and thus be heterozygous for the trait. When an individual is homozygous, the corresponding trait will be expressed. When an individual is heterozygous for a trait, the instructions of the dominant allele will be expressed (see Figure 3.3). FIGURE 3.3 Mendelian inheritance patterns Pictured here are the Mendelian inheritance patterns for the offspring of two brown-haired parents who are both heterozygous for hair colour. The allele for brown hair (B) is dominant and that for blond hair (b) is recessive. Note that these parents have three chances out of four of producing children with brown hair. They have two chances in four of producing brown-haired children who carry the gene for blond hair. The sex chromosomes present an interesting wrinkle in the story of dominance patterns. The X chromosome carries roughly 1500 genes, whereas the much smaller Y chromosome carries only about 200. Thus, when a genetically female child inherits a recessive allele on the X chromosome from her genetically female parent, she is likely to have a dominant allele on the
avoided contact with strangers; her temperament limited the types of interactions she had with unfamiliar adults. Thus, these two children, despite living in the same home with the same parents, experienced very different early environments by virtue of their own behaviours. Children also create their own environments by actively selecting surroundings and experiences that match their interests and personalities. As soon as infants start reaching, crawling, and walking, they begin to select objects for exploration rather than relying on their parents’ choices of play objects. Beginning in the preschool years, children choose playmates whom they enjoy and activities that interest them. Returning to the reading example, children who enjoy books will read more than children who find reading tedious. The more they read, the more skilled they become, leading them to choose increasingly more challenging books; this, in turn, leads them to acquire advanced vocabulary, improve their language comprehension, and enhance their general knowledge base, resulting in greater success in school. Children’s ability to shape their own environments has profound effects on intellectual development, as we will see in Chapter 8. 5 Child’s Environment–Child’s Genotype The fifth relationship in our model is perhaps the most surprising. Geneticists previously believed that the genotype was “fixed” at conception. But as discussed in Chapter 1, the field of epigenetics has turned this conventional wisdom on its head. Although the structure of the genetic code remains “fixed” during one’s lifetime, the expression of the genetic code is altered. Recall that a specific gene does not lead to a specific phenotype but that, instead, the genetic encoding of proteins alters the ways in which genes are expressed as phenotypes. Epigenetic mechanisms, mediated by the environment, can alter the functioning of genes and create stable changes in their expression—and some of these changes can be passed on to the next generation.
The epigenetic mechanism most commonly studied in humans is methylation, which silences gene expression. Methyl molecules block transcription in the promoter region of the gene, turning off gene activity, as illustrated in Figure 3.5. DNA methylation typically operates like a dimmer switch, regulating the amount of protein produced by a given gene (Lester, Conradt, & Marsit, 2016). Epigenetic processes involving methylation are of particular interest to developmental scientists because they provide evidence for long-term epigenetic effects of early adverse experiences on gene expression, impacting later health and well-being (e.g., Provenzi et al., 2016).
Key evidence for how methylation exerts epigenetic effects on behaviour comes from studies of rodents. Like humans, rodent mothers vary in the quality of their maternal behaviour. Typical rat mothering involves licking and grooming behaviour, which activates glucocorticoid receptor genes (recall from Chapter 2 that glucocorticoids are involved in stress reactivity). But some rat mothers do not perform these maternal behaviours at the same rate—a nonhuman analogue to human child neglect. And indeed, research at McGill University found that rat pups whose mothers were unresponsive show less activity in the glucocorticoid receptor gene (Weaver et al., 2004). As adults, these rat offspring were more fearful and showed aberrant stress responses. Because they were working with rats, the research team was able to use a research design that is not possible with human infants: they cross-fostered the rat pups, assigning some of the pups to be raised by mothers to whom they were genetically unrelated. This manipulation allowed the researchers to show that the effects they observed—stable alternations of DNA methylation as a function of maternal behaviour—were truly due to the rat pups’ postnatal environments, rather than to prenatal or genomic differences.
As you saw in Chapter 1, early stress also affects methylation in humans (e.g., Conradt, 2017). For example, children who experienced severe early-life stress in the form of child maltreatment show similar patterns of methylation in the glucocorticoid receptor gene as the rodents who received poor parental care (Romens et al., 2015). Other researchers used a whole-genome screen to examine both methylation and gene expression in a group of 9- to 12-year-old girls who had experienced levels of childhood adversity ranging from mild to severe (Papale et al., 2018). The results revealed a large number of genes (more than 100!) whose methylation levels varied in association with the amount of stress the girls had experienced. Another study revealed epigenetic changes related to childhood abuse in the sperm cells of adult males—cells that are of particular interest as a possible mechanism for passing epigenetic changes from parent to child (Roberts et al., 2018). Given all of the genetic reshuffling that occurs at conception, as discussed earlier in this chapter, much of the methylation in germ cells is erased. Nevertheless, this research suggests a possible epigenetic route for the cross-generational transmission of stress. Our discussion of the relationships between genotypes, phenotypes, and environments emphasized the challenges in understanding how genes impact the development of individuals. Nevertheless, the conceptualization we have presented is greatly simplified. This is particularly true for the fifth relationship—epigenetics—which, when considered in full, suggests that the line between genes and environment is blurry at best. In the next section, we will explore the research designs and tools that researchers in the field of behaviour genetics have used to make headway in teasing apart nature and nurture in the study of human development.
Behaviour Genetics Why do the individuals in any group of human beings vary in terms of how smart, sociable, depressed, aggressive, and religious they are? Researchers in the field of behaviour genetics assume that all behavioural traits are, to some extent, heritable. Individual differences in a trait, therefore, are influenced to some degree by genetically transmissible factors (e.g., Plomin, 2018). Behaviour geneticists try to tease apart genetic and environmental contributions by taking advantage of the differences observed amongst a population. Two premises underlie this endeavour: (1) To the extent that genetic factors are important for a given trait or behaviour, individuals who are genotypically similar should be phenotypically similar; and (2) to the extent that shared environmental factors are important, individuals who were reared together should be more similar than people who were reared apart. Quantitative Genetics Research Designs Quantitative behaviour geneticists use statistical methods to study “naturally occurring genetic and environmental variation” in a population by comparing the phenotypes of individuals who vary in the amount of genomic DNA they share (Plomin, DeFries, & McClearn, 2008, p. 70). The mainstay of quantitative behaviour genetics is the family study, which attempts to determine whether phenotypic traits are correlated with the degree to which people are genetically related—parents and children, identical and fraternal twins, non-twin siblings, or adoptive family members. (As you may recall from Chapter 1, the strength and direction of a correlation indicate the extent to which two variables are related; the higher the correlation, the more precisely scores on one variable can be predicted from scores on the other.) The resulting correlations are compared to see if they are (1) higher for more closely related individuals than for less closely related people, and (2) higher for individuals who share the
same environment than for individuals who do not. The twin-study design is a specialized form of the family study used to compare the correlations for identical (monozygotic, or MZ) twins with those for same-sex fraternal (dizygotic, or DZ) twins. As you will recall, identical twins have 100% of their genes in common (though gene expression is affected by epigenetic factors, as discussed in the preceding section), whereas fraternal twins share, on average, 50% of their genomic DNA (just like non-twin siblings). For twins who grow up together, the degree of similarity of the environment is generally assumed to be equal. Known as the equal environments assumption, the claim is that both types of twins shared the same prenatal environment, were born at the same time (so experienced societal changes similarly), grew up in the same family and community, and are always the same age when tested. If the correlation between identical twins on a given trait or behaviour is substantially higher than that between fraternal twins, it is assumed that genetic factors are substantially responsible for the difference. Video: Genes and Personality
It is important to note, however, that the equal environments assumption has been questioned (e.g., Felson, 2014; Richardson & Norgate, 2005). For example, parents of MZ twins may treat them more similarly than parents of DZ twins. And even amongst MZ twin pairs, there are notable differences in the degree of placental sharing (known as chorionicity), complicating measures of prenatal environmental similarity (Van Beijsterveldt et al., 2016). While many MZ twin pairs fully share a placenta, others do not, making their prenatal environments more akin to those of DZ twins. And, of course, the idiosyncratic experiences of MZ twins may differ—for example, one twin may end up with higher-quality or more engaging teachers than the other. Thus, it is overly simplistic to assume that environments of MZ twin pairs and DZ twin pairs are always equally similar to one another. Another family-study design is the adoption study. In this approach, researchers examine whether adopted children’s scores on a given measure are correlated more highly with those of their biological parents and siblings or with those of their adoptive parents and siblings. Genetic influences are inferred to the extent that children resemble their biological relatives more than they do their adoptive ones. We began this chapter with the ideal behaviour genetics design—the adoptive twin study—in which identical twins who grew up together are compared to identical twins who were separated shortly after birth and raised apart. If the correlations for twins reared apart are similar to those for twins reared together, it suggests that environmental factors have little effect. Conversely, to the extent that the correlations between identical twins who grew up in different environments are lower than those for identical twins who grew up together, environmental influence is inferred. As we mentioned earlier, however, children’s phenotypes also shape their environments (Relations 2 and 4). Furthermore, adoption agencies generally place separated twins with families of backgrounds similar to one another. Therefore, even adoptive twin study designs are vulnerable to confounding of environmental and genetic factors. Twin studies compare correlations for identical twins (top) and same-sex fraternal twins (bottom) to estimate the heritability of a given trait. Heritability To estimate how much of the variability in measures of a given trait is attributable to genetic and environmental factors, behaviour geneticists derive heritability estimates from correlations of the type shown in Table 3.1. Heritability is a statistical estimate of how much of the measured variance on a phenotypic trait amongst individuals in a given population is attributable to genetic differences amongst those individuals. Heritability analyses have been applied to many diverse aspects of human behaviour, several of which you will encounter in other chapters of this book. One large meta-analysis of more than 17,000 traits—with more than 14 million twin pairs—found that heritability was greater than zero for every trait investigated in the analysis (Polderman et al., 2015). These traits include psychological traits like temperament, which we will discuss further in Chapter 10, as well as many other aspects of personality, cognition, and psychopathology (Plomin et al., 2016; Vukasović & Bratko, 2015). One well-studied trait is intelligence. Table 3.1 summarizes the results of more than 100 family studies of IQ through adolescence. The pattern of results reveals both genetic and environmental influences. Genetic influence is revealed by the presence of generally higher correlations for individuals with higher degrees of genetic similarity. Most notable is the finding that identical (MZ) twins resemble each other in IQ more than do same-sex fraternal (DZ) twins. At the same time, environmental influences are reflected in the fact that identical twins are not identical in terms of IQ. Further evidence for the influence of environmental factors is that MZ twins reared together are more similar than those reared apart.
As compelling as they seem, heritability measures have also been widely criticized. Part of the criticism stems from ways that the term heritability is often misinterpreted or misused by the public. The concept of heritability is commonly (and mistakenly) applied to individuals, despite the fact that, as we have emphasized, heritability applies only to populations. The heritability of intelligence, for example, is generally considered to be approximately 50%. This means that, for the population studied, roughly 50% of the variation in IQ scores is due to genetic differences amongst the members of the population. It does not mean that 50% of your IQ score is due to your genetic makeup and 50% is due to your experience. Furthermore, a heritability estimate applies only to a particular population living in a particular environment. Consider the case of height. Research conducted almost exclusively with North Americans and Europeans—most of them adequately nourished—puts the heritability of height at around 90%. But what if some segment of this population had experienced a severe famine during childhood, while the rest remained well fed? Would the heritability estimate for height still be 90%? No—because the variability due to environmental factors (poor nutrition) would increase dramatically; therefore, the variability that could be attributed to genetic factors would decrease to the same degree. Another common misperception is that heritability estimates are inherent to the trait in question and are not affected by the context in which the trait is measured. But heritability estimates necessarily reflect the environments of the populations of individuals from which they are derived. Consider hypothetical heritability estimates of reading ability for children in two different countries: Brazil, where there is considerable variability in educational opportunities, and Finland, where nearly all children have the same excellent educational opportunities (Bishop, 2015). The heritability estimate of reading ability for children in Brazil would likely be much lower than in Finland. For children in Brazil, individual differences in reading outcomes will be more heavily influenced by the environment because educational experiences are far more variable than in Finland. Thus, heritability estimates may appear larger within populations with more homogeneous environments. A related observation is that even for the same trait in the same population, heritability estimates can change as a function of developmental factors. Sometimes these patterns are counterintuitive. For instance, as twins get older, the degree of variance in intelligence accounted for by their genetic similarity actually increases (Haworth et al., 2010). These results are consistent with the idea that people actively construct their own environment: the phenotype–environment correlation (Relation 4) discussed earlier. Younger children have little
playground—can contribute further to the development of individual differences amongst siblings. Much like the action of polygenic inheritance patterns, in which many genes of small effect work together to influence development, the effects of the environment are likely due to many experiences of small effect working together. A final observation is that environments are much harder for researchers to measure than genes. Complex phenotypes of interest to developmental scientists (cognitive abilities, personality, psychopathology) are also notoriously difficult to assess in the context of large-scale experiments. In the next section, we will see how a better understanding of brain development is helping to answer some of these questions.
Brain Development The collaboration between nature and nurture takes centre stage in the development of the brain and nervous system. The Neuron The basic units of the brain’s remarkably powerful informational system are its more than 100 billion neurons (depicted in Figure 3.6), which constitute the grey matter of the brain. Each neuron has three main components: (1) a cell body, which contains the basic biological material that keeps the neuron functioning; (2) dendrites, fibres that receive input from other cells and conduct it towards the cell body in the form of electrical impulses; and (3) an axon, a fibre (anywhere from a few micrometres to more than a metre in length) that conducts electrical signals away from the cell body to connections with other neurons. Neurons communicate by sending electrical and chemical signals across synapses, microscopic junctions between the axon terminal of one neuron and the dendritic branches of another. There are hundreds of trillions of synapses in the human brain, with some neurons having as many as 15,000 synaptic connections with other neurons.
Glial cells are another essential component of the brain, equal in numbers to neurons (von Bartheld, Bahney, & Herculano-Houzel, 2016). Glial cells perform a variety of critical functions, including the formation of a myelin sheath around axons, which increases the speed and efficiency of information transmission. Glial cells also function as neural stem and progenitor cells during prenatal brain development, and some glial cells continue to do so into adulthood. When the brain is injured, some glial cells react by rapidly increasing in numbers, protecting the brain and potentially aiding in regeneration. The Cortex The cerebral cortex constitutes 80% of the human brain, a much greater proportion than in other species. The folds and fissures visible in Figure 3.7 form as the brain grows within the confined space of the skull; these convolutions make it possible to pack more cortex into the limited space. The parts of the human cortex that are most enlarged compared with other species are also those that grow the most as children develop.
The cortex includes four lobes, each associated with a specific set of behavioural characteristics. Starting at the back of the brain, the occipital lobe is primarily involved in processing visual information. The temporal lobe is associated with speech and language, and the processing of emotion and auditory information. The parietal lobe engages in spatial processing and is also involved in the integration of information from different sensory modalities. The frontal lobe, the brain’s “executive,” is involved in cognitive control, including working memory, planning, decision-making, and inhibitory control. Information from multiple sensory systems is processed and integrated in the association areas that lie in between the major sensory and motor areas. Complex mental functions are mediated by multiple areas of the brain, with an extraordinary degree of interactivity both within and across brain regions. (Box 3.3 examines some of the techniques that developmental scientists use to study brain functioning.) The cortex is divided into two cerebral hemispheres. For the most part, sensory input from one side of the body goes to the opposite side of the brain, and the motor areas of the cortex control movements of the opposite side of the body. The hemispheres communicate with each other primarily by way of the corpus callosum, a dense tract of connective nerve fibres between the two hemispheres. The hemispheres are specialized for different modes of processing, a phenomenon referred to as cerebral lateralization. Lateralization emerges early in human development. For example, young infants use their right hemispheres more than their left hemispheres to process faces (Adibpour, Dubois, & Dehaene-Lambertz, 2018), and their left hemispheres more than their right hemispheres to process most aspects of speech (e.g., Dehaene-Lambertz, 2017). However, contrary to popular belief, people are not left brained or right brained; individuals do not tend to have a general preference to use one hemisphere over the other (e.g., Nielsen et al., 2013).
Neurogenesis and Neuron Development Neurogenesis, the proliferation of neurons through cell division, begins 42 days after conception (in humans) and is nearly complete by the midway point of gestation (Stiles & Jernigan, 2010). Thus, most of the roughly 100 billion neurons you currently possess have been with you since before you were born. Notably, however, humans do continue to generate new neurons throughout life, particularly in the hippocampus—a brain area that is heavily involved in memory processes (Kempermann et al., 2018). As you will see, neurogenesis is one of several ways in which experiences sculpt the brain. After their “birth,” neurons migrate to their ultimate destinations—typically outwards from the centre of the brain towards the developing neocortex. Some neurons are pushed along passively by the newer cells formed after them, whereas others actively propel themselves towards their ultimate location. Once neurons reach their destination, they first grow an axon and then a “bush” of dendrites (refer back to Figure 3.6). Thereafter, they take on the specific structural and functional characteristics of the different structures of the brain. Axons elongate as they grow towards their targets. The main change in dendrites is arbourization—an enormous increase in the size and complexity of the dendritic “tree” that results from growth, branching, and the formation of spines on the branches. Arbourization increases the dendrites’ capacity to form connections with other neurons, as illustrated in Figure 3.8. As arbourization allows neurons to grow in complexity over the first several years of postnatal life, the cortex grows in surface area and the layers of the cortex become thicker (e.g., Gilmore et al., 2018).
Myelination, the formation of the insulating myelin sheath around some axons, begins prenatally and continues into early adulthood. The myelinated portions of axons are white, leading to the term white matter, and lie below the grey matter (cell bodies) at the surface of the cortex. Myelination begins deep in the brain and moves upwards and outwards into the cortex. This process occurs rapidly for the first few months after birth, slows somewhat during toddlerhood, and continues slowly into young adulthood (e.g., Dubois et al., 2014). The various cortical areas become myelinated at very different rates, contributing to the different rates of maturation of different brain areas; for example,
the sensory areas in the back of the brain mature much sooner than the executive function areas in the front of the brain, as shown in Figure 3.9.
Synaptogenesis The extraordinary growth of axonal and dendritic fibres results in a wildly exuberant generation of neuronal connections. Each neuron forms synapses with thousands of others in a process called synaptogenesis, resulting in the formation of the trillions of connections referred to earlier. Figure 3.10 shows the course of synaptogenesis in the cortex over time. As you can see, it begins prenatally and proceeds very rapidly both before birth and for some time afterwards. Note that both the timing and rate of synapse production vary for different cortical areas; synapse generation is complete much earlier in sensorimotor cortex, for example, than in the frontal area. As with myelination, the differential timing of synapse generation across areas of the brain likely contributes to the developmental timing of the onset of various abilities and behaviours.
Synapse Elimination The explosive generation of neurons and synapses during synaptogenesis results in many more neural connections than any one brain can use. Approximately 40% of this great synaptic superfluity is eliminated through synaptic pruning, which occurs at different times in different areas of the brain, as shown in Figure 3.10. The brain undergoes waves of synaptogenesis and synaptic pruning in the first months and years of life, but the brain also undergoes substantial changes during adolescence—in fact, measures of cortical thickness suggest that the outer layers of the cortex shrink at a faster rate during adolescence than during either childhood or early adulthood (Whitaker et al., 2016). The last area of the cortex to mature is the dorsolateral prefrontal cortex, which is vital for regulating attention, controlling impulses, foreseeing consequences, setting priorities, and other executive functions (refer back to Figure 3.9). It does not reach adult dimensions until after the age of 20, and synaptic pruning continues until individuals are in their 30s (Petanjek et al., 2011).
Atypical patterns of pruning have been implicated in two developmental disorders: autism spectrum disorder (ASD) and schizophrenia. Autistic children have larger brains than neurotypical children, and studies suggest that autistic children and adults have greater synaptic densities in some areas of their brains (e.g., Neniskyte & Gross, 2017). There is also evidence for increased cortical thickness in autistic children relative to neurotypical children, possibly indicating reduced or delayed rates of synaptic pruning (Khundrakpam et al., 2017). Patterns of neural connection in individuals with schizophrenia also follow an atypical trajectory and suggest excessive pruning in adolescence (e.g., Johnson & Hyman, 2022). As discussed earlier, there is typically a burst of synaptic pruning around adolescence, especially around the prefrontal cortex. The timing of the onset of schizophrenic symptoms in adolescence and young adulthood may be linked to aberrant pruning around puberty.
The Importance of Experience What factors determine which of the brain’s excess synapses will be pruned and which maintained? Experience plays a central role in what is essentially a case of “use it or lose it.” The more often a synapse is activated, the stronger the connection between the neurons involved: in short, neurons that fire together wire together (Hebb, 1949). Conversely, when a synapse is rarely active, it is likely to disappear: the axon of one neuron withdraws and the dendritic spine of the other is pruned away.
The process of massive overproduction of synapses, followed by selective pruning, is the brain’s answer to a fundamental tension between rigidity and flexibility. Because of the brain’s capacity to be molded or changed by experience, referred to as plasticity, less information needs to be encoded in the genes. This evolutionary economizing may, in fact, be a necessity: the number of genes involved in the formation and functioning of the human nervous system is enough to specify only a very small fraction of our neural connections. In addition, if brain structures were entirely hardwired, organisms would be unable to adapt to their environments. The plastic brain can recover from some forms of injury because other brain areas can take over the function that would have been performed by the damaged area. Because children’s brains are more plastic than adults’ brains, children who sustain brain damage have a better chance of recovering lost function than do adults who sustain similar damage. A particularly striking example arises when comparing the effects of strokes at different ages on language processing. Recall that most aspects of language are typically processed in the left hemisphere (for right-handed individuals). Infants who experience perinatal strokes that damage their left hemisphere around the time of birth show a remarkable ability to learn language using their right hemisphere. When tested as young adults, even participants who lost essentially their entire left hemisphere due to perinatal stroke show normal sentence-processing abilities (Newport et al., 2022). In contrast, adults who sustain the same type of brain damage undergo minimal reorganization of language functions and may lose some language abilities permanently. The collaboration between nature and nurture in building the brain occurs differently for two kinds of plasticity. Experience-expectant plasticity involves the general experiences that almost all infants have just by virtue of being human. Experience-dependent plasticity involves specific, idiosyncratic experiences that children have as a result of their particular life circumstances—such as growing up in Montréal or in the Amazon rain forest, experiencing frequent cuddling or abuse, and so on.
Experience-Expectant Processes The role of species-typical experience in shaping brain development is known as experience-expectant plasticity (Greenough, Black, & Wallace, 1987). Each species evolves in a particular environmental niche, with a predictable array of experiences available to all typically developing members of that species. The specific circumstances and experiences under which a species evolves impacts how their brain development unfolds. For example, throughout human evolution, infants have experienced patterned visual stimulation, voices and other sounds, movement and manipulation, and so forth. The human brain can thus “expect” that these sources of experience will be available to fine-tune its circuitry—hence the term experience-expectant plasticity. The benefit of experience-expectant plasticity is that, because experience helps shape the brain, fewer genes need to be dedicated to normal development. That is, less information needs to be preinstalled in the brain. The downside is heightened vulnerability. If the experience that the developing brain “expects” does not occur, development may be compromised. This phenomenon is exemplified by the classic work of Hubel and Wiesel, who deprived kittens of light exposure in one of their eyes (Hubel & Wiesel, 1962, 1970; Wiesel & Hubel, 1963). When the eye was
offspring (Lorenz, 1971). And indeed, studies suggest that the reward circuitry in human adults’ brains is activated by infant cuteness traits (Glocker et al., 2009). Video: Physical Development in Infancy and Toddlerhood Across species, infants display disproportionately large heads, high foreheads, and large eyes, as seen in this photo of a human infant and puppy. Variability There is great variability across individuals in all aspects of physical development. Genes affect growth and sexual maturation by influencing the production of hormones, especially growth hormone (secreted by the pituitary gland) and thyroxine (released by the thyroid gland). The influence of environmental factors is particularly evident in secular trends, marked changes in physical development that have occurred over generations. In contemporary industrialized nations, adults are several inches taller than their great-grandparents were. This change is assumed to have resulted primarily from improvements in nutrition and general health. Conversely, children raised in institutions have a higher risk of growth impairment, likely due to both stress and poor nutrition (Johnson & Gunnar, 2011). For example, when children from Romanian orphanages arrived in their adoptive homes in Canada, their average weight was below the 4th percentile. About 8 years after adoption into their Canadian homes, these children had caught up considerably in growth. At 10 1 2 years of age, the Romanian adoptees’ average weight was around the 60th percentile and was no longer significantly different from that of Canadian-born, never-adopted children (Le Mare & Audet, 2006). Another secular trend that has emerged over the past few decades is that girls, on average, begin menstruating a few years earlier than their ancestors. This is particularly true of girls growing up in low-SES families. For example, 11-year-old British girls living in poverty were twice as likely as their peers in wealthy households to have begun menstruating (Kelly et al., 2017). Obesity and stress are both predictors of early menstruation.
Nutritional Behaviour The health of our bodies depends on what we put into them. The development of nutritional behaviour is a crucial aspect of child development from infancy onwards. The North American infant formula shortage in 2022—where product recalls and supply chain issues severely limited the availability of infant formula—spoke directly to the challenges entailed in ensuring safe nutritional options for infants. Infant Feeding Throughout nearly the entire history of the human species, the primary source of nourishment for infants was breast milk. It is naturally free of bacteria and contains the breast-feeding parent’s antibodies against infectious agents the baby is likely to encounter. Breast-feeding is also good for the health of breast-feeding parents: amongst other benefits, breast-feeding decreases the parent’s risk of breast and ovarian cancer. There have also been suggestions in the literature that the fatty acids in breast milk have a positive effect on cognitive development. A number of studies indicate higher IQ scores for children and adults who were breast-fed as infants, even after controlling for parental IQ (for review, see Kanazawa, 2015; Nisbett et al., 2012). These effects may be mediated by increased myelination in breast-fed infants, which, as discussed earlier in this chapter, increases efficiency of information transmission in the nervous system (Deoni et al., 2018). Other studies suggest that while there are long-term cognitive benefits of breast-feeding, they are relatively minor (e.g., Boutwell, Young, & Meldrum, 2018). Research findings in this area can be difficult to interpret because breast-feeding is linked with SES and household food insecurity in Canada (Orr et al., 2018), and SES is also correlated with IQ. In spite of the well-established nutritional superiority of breast milk, many infants around the world are formula-fed. One factor that leads many parents to forgo breast-feeding, as noted previously, is the lack of access to paid parental leave. Numerous studies have revealed a relationship between paid leave and breast-feeding prevalence around the world (Baker et al., 2023)—in Canada, to take one example, an increase in paid maternity leave from 6 to 12 months correlated to a 40% increase in the proportion of parents who exclusively breast-fed their infants (Baker & Milligan, 2008). The number of hours a day that a breast-feeding parent devotes to nursing and/or pumping can also act as a deterrent when weighed against the financial cost of that time. One study using data from the 1980s found that women in the United States who breast-fed for more than 6 months experienced greater earnings loss over the ensuing 5 years than those who did not breast-feed or who breast-fed for less than 6 months (Rippeyoung & Noonan, 2012). Finally, breast-feeding is physically challenging, often extremely so. New parents who desire to nurse their infants may struggle with milk production or latching (attaching to the breast and withdrawing milk), leading to difficult decisions about how best to feed their infant. In Canada, efforts to promote breast-feeding have included public-health campaigns and access to lactation consultants who can support parents as they face challenges in breast-feeding. These efforts have paid off as over 90% of neonates receive breast milk, proportions higher than in Australia, the United Kingdom, and the United States (Statistics Canada, 2022e). However, this good nutritional start is difficult for parents to maintain; by 4 months of age, only 56% of infants in Canada are exclusively breast-fed, and by 6 months of age the number drops down to 34%. Despite these challenges, breast-feeding rates in Canada are high relative to some other high-income countries like the United Kingdom, where in England and surrounding areas only 49% of 1-month-olds were breast-fed in 2022 (Public Health England, 2022). Breast-feeding rates are much higher in lower-income countries in sub-Saharan Africa, South America, and Southeast Asia, where the majority of infants are breast-fed until at least 1 year of age (Victora et al., 2016). In these countries, infant formula is often mixed with polluted water in unsanitary containers; thus, breast-feeding is especially important in promoting positive health outcomes in countries with unsafe drinking water and fewer public health resources.
Development of Food Preferences Food preferences impact what we eat throughout life, and some of these preferences are innate. Infants display some of the same reflexive facial expressions that older children and adults display in response to basic tastes: sweet, umami (savoury), bitter, sour, and salty (e.g., Ventura & Worobey, 2013). The first two flavours produce positive responses: a hint of a smile, lip smacking, sucking. Bitter flavours elicit negative responses, including frowning and nose wrinkling. Sour flavours elicit varied responses: some infants respond negatively while others respond positively. Salty flavours do not elicit much of a reaction until after 4 months of age, when a preference for salt emerges. Newborns’ strong preference for sweetness is reflected both in their positive response to sweet flavours and in the fact that they will drink larger quantities of sweetened water than plain water. These preferences may have an evolutionary origin, because poisonous substances are often bitter or sour but almost never sweet. At the same time, recall from Chapter 2 that taste preferences can also be influenced by the prenatal environment, suggesting an important role for experience even in the earliest flavour preferences. Breast milk also takes on some of the flavours of the foods that nursing parents eat.
The rapid transition out of a primarily liquid diet brings a variety of opportunities and challenges. Most young children demonstrate food neophobia: an unwillingness to eat unfamiliar foods. Avoidance of unknown foods likely evolved as an adaptive response, helping to keep children safe (especially important given infants’ and toddlers’ propensity to put everything they find in their mouths). Research suggests that the best way to overcome children’s conservative eating tendencies is to repeatedly introduce new foods, ideally between 6 and 15 times over the course of a few weeks (Ventura & Worobey, 2013). This exposure should include tasting; just seeing a novel food is insufficient to override children’s wariness. For older children, simply being involved in preparing a specific dish increases their intake of that food, at least in the short term (DeJesus et al., 2019). Pressuring children to try new foods, or bribing them (“If you have two bites of broccoli, you can have dessert”), is likely to backfire. By pairing foods in this fashion, parents send the message that broccoli is punishment while dessert is the reward. Parents also inadvertently increase the value of foods by restricting them. When access to certain foods is limited, children will tend to overindulge when they have the opportunity to do so (e.g., Ventura & Worobey, 2013). More generally, parental use of food as a way to control children’s behaviours and emotions is a predictor of risk factors for obesity (e.g., Larsen et al., 2015). Eating is an inherently social act, and much of what children learn about food comes from observing others (in Chapter 9, we will discuss the role of observational learning in social development more generally). Toddlers are more likely to accept novel foods from a caregiver than from a stranger. They are also more likely to choose foods endorsed by others who are similar to them along key social dimensions, including gender and native language (Shutts, Kinzler, & DeJesus, 2013). Indeed, infants expect individuals from their social group to share food preferences—but not preferences for nonfood items such as novel objects, suggesting that even infants understand that food choices reflect social conventions (Liberman et al., 2016). Associative learning, which we will discuss in Chapter 5, also influences children’s food choices. Foods marketed to young children are often branded with popular cartoon characters (e.g., those from Sesame Street) and mascots (e.g., Tony the Tiger). Furthermore, as shown by a Canadian study, these foods tend to be of poor nutritional quality (Elliott & Scime, 2019). This branding strategy makes a difference: children are more likely to select, and rate more highly, foods that are branded with familiar characters (e.g., Kraak & Story, 2015). Child-targeted marketing, including pairing unhealthy foods with enticing toys as part of kid meals at fast-food restaurants, is one contributor to childhood obesity. Indeed, merely telling 5- and 6-year-olds that a food is popular with other children leads them to consume more of it (DeJesus, Shutts, & Kinzler, 2018)! In response to concerns about food marketing to children, Health Canada is working to restrict the marketing of unhealthy foods and drinks to children as part of their healthy eating strategy (Health Canada, 2019).
Associative learning can also be used to encourage healthy choices. One study used branding to market the salad bars in elementary school cafeterias in a large urban school district (Hanks, Just, & Brumberg, 2016). By simply fastening to the salad bar a banner that showed cartoon vegetable characters, the number of students who chose vegetables doubled. When the banner was paired with television advertisements featuring the vegetable characters, the number of students who chose vegetables tripled. Thus, advocates of healthy eating should consider taking advantage of the marketing tools that have so long predominated in the advertising of unhealthy options. Obesity In Canada, around 12% of children and adolescents are considered obese (Molina et al., 2023) but childhood obesity is a global problem, with 380 million overweight and obese children and adolescents worldwide (World Health Organization, 2021). The majority of these children live in developing countries, which have shown a particularly steep rate of increase in obesity, as can be seen in Figure 3.11. This situation exists largely because societies all over the world are increasingly adopting a “Western diet” of foods and drinks high in fat and sugar and low in fibre, due in part to the ever-increasing penetration of global fast-food chains, paired with less physical activity in an increasingly urbanized world.
Evidence from around the world indicates that obesity rates may have increased during the pandemic. For example, separate studies in Philadelphia and in Israel each found a 2% increase in childhood obesity rates from 2019 to the end of 2020 (Jenssen et al., 2021; Shalitin, Phillip, & Yackobovitch-Gavan, 2022). Pandemic-related day-care and school closures in 2020 and 2021 cut children off from a source of both appropriately portioned meals and opportunities for physical activity, as well as increased opportunities for unhealthy snacking, sleep dysregulation, screen time, and stress—all of which affect physical health.
Two important questions need to be addressed: Why do some people but not others become overweight, and why is obesity so prevalent? Again, both genetic and environmental factors play roles. Genetic factors are reflected in the findings that (1) the weight of adopted children is more strongly correlated with that of their biological parents than with that of their adoptive parents, and (2) identical twins, including those reared apart, are more similar in weight than fraternal twins are (Plomin et al., 2012). Research on dogs has revealed a specific genetic deletion (POMC), occurring in breeds with high rates of obesity, associated with weight and appetite that causes these dogs to be hungrier than others (Raffan et al., 2016). The POMC gene is present in humans also, and, in rare cases, deficiencies lead to human obesity. However, GWAS studies suggest that, like most other complex traits, human obesity risk is polygenic (Tung et al., 2014). While no single gene predicts obesity, genes affect individuals’ susceptibility to gaining weight and how much food they eat in the first place. A host of environmental factors fuel childhood obesity. Schools provide cafeteria lunches consisting of high-fat foods and drinks. Canadian children today also spend far less time playing outside, and they are less likely to walk or bike to school than their counterparts in previous generations. Children spend increasingly more hours per day with screens (a trend that we will discuss in Chapter 9), and amount of screen time is associated with obesity (e.g., Fang et al., 2019). Children who get less sleep are more prone to obesity, as are children with screens in their rooms (which may also detract from sleep duration; Appelhans et al., 2014; Wethington, Pan, & Sherry, 2013). Finally, unhealthy foods are often cheaper and more readily available than healthier foods, especially in urban and rural areas that lack full-service supermarkets. In such areas, known as “food deserts,” residents often must rely on convenience stores that stock primarily high-calorie prepackaged foods, making it more difficult for parents to provide healthy foods for their children.
Obesity puts children and adolescents at risk for a wide variety of serious health problems, including heart disease and diabetes. In addition, many obese youth suffer the consequences of negative stereotypes and discrimination in a variety of areas. As early as grade 1, children
associated with the COVID-19 pandemic limited children’s access to health care and disrupted mass immunization campaigns around the world, leading to a marked drop in immunization rates for preventable childhood diseases (World Health Organization, 2022). In addition to these logistical challenges, some parents believe that vaccines will harm their children. In a highly publicized study in the 1990s, a British physician claimed that autism is caused by the MMR vaccine routinely given to young children to prevent measles, mumps, and rubella (Wakefield et al., 1998). It was subsequently discovered that this paper was fraudulent, and it has since been retracted by the journal that published it (Godlee, Smith, & Marcovitch, 2011). Subsequent research has found no link between vaccines and autism (Hviid et al., 2019; Jain et al., 2015; McMahon et al., 2008; Price et al., 2010). The decision by some parents to refuse MMR and other important vaccines creates a risk for both their children and others in the community. Because vaccines operate based on herd immunity, a certain percentage of the population must be immunized in order to protect the population. In Canada, vaccination is only mandatory for enrollment in public school in Ontario and New Brunswick, and in these provinces, parents can exempt their children for religious or philosophical reasons. By voluntarily removing their children from the vaccinated population, parents risk dropping vaccine rates below the level needed for herd immunity, a particular problem for those children who cannot be vaccinated due to age or medical conditions (e.g., cancer patients who are immune-compromised). These actions can have serious consequences, as in the cases of outbreaks in 2020–2022 of measles, polio, and other diseases targeted by vaccines, possibly due to decreased access to health care related to the COVID-19 pandemic lockdowns. The COVID-19 pandemic prompted an increased focus on vaccines. Discussions about vaccination became highly politicized after the vaccines became broadly available in 2021. At that time, 45% of parents of young children (2 years to 4 years) in Canada reported that they would vaccinate their children against COVID-19, indicating that they wanted to protect their child and family from becoming ill (Humble et al., 2022). Parents who were undecided or who did not intend to vaccinate their child reported concerns about vaccine safety, the speed of vaccine development, and the newness of the vaccine. Notably, these safety concerns are inconsistent with the data. The systems used to track adverse reactions to vaccines in Canada show vanishingly small numbers of serious side effects in young children (Public Health Agency of Canada, 2023). Importantly, the vaccines appear to be quite effective in decreasing the likelihood of symptomatic COVID-19 for young children under 5 years of age, reducing risk by over 70% relative to unvaccinated children (Muñoz et al., 2023). These recent debates have impacted how parents think about other vaccines. In the United States for example, most parents (80%) agree that the benefits of the classic childhood MMR vaccine outweigh its risks—a rate that has remained largely unchanged in recent years (Lopes et al., 2022b). However, a favourable view of the MMR vaccine doesn’t necessarily translate into a favourable view of other vaccines; for example, 70% of parents who chose not to get the COVID-19 vaccine agree that the benefits of the MMR vaccine for children outweigh its risks. Furthermore, 60% of these adults also believe that parents should be able to decide not to vaccinate their children for MMR, even if that may increase health risks for other people. In some parts of the world, vaccination is hampered by cost and logistical challenges. For example, vaccines need to be kept cold, which poses a problem in communities with irregular access to electricity. One innovative approach is being implemented in Vanuatu, a nation made up of 83 small islands in the South Pacific. About 20% of the children in Vanuatu do not receive all of their vaccinations due to the remoteness of villages and lack of electricity. To address this problem, UNICEF funded a program to deliver vaccines by drone. Each drone can hold a 5-pound pack of vaccines packaged in ice and can fly 30 miles to villages that are difficult to reach by road or sea. This program represents a clever use of modern technology to deliver lifesaving vaccines, and it was implemented more recently to deliver COVID-19 vaccines to remote locations in India and other countries.
