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In this chapter we step back from the numerous analyses described in previous chapters in order to gain some perspective on what we know and what we need to learn about the origins of individual differences during infancy and early childhood. As presaged in Chapter 1, the ratio of what is known to what is not known is small; however, the ratio is more impressive when we consider how few studies have addressed the issue of the origins of individual differences in infancy and childhood.
Principles
Rather than summarizing the preceding chapters, we have attempted to abstract some principles that outline what is known about nature and nurture in infancy and early childhood. In our book on infancy, several principles were drawn from the infancy results of the Colorado Adoption Project (Plomin & DeFries, 1985a). These principles involve some general points, such as the following. The etiology of individual differences in infancy includes heredity, variations in family environment are related to individual differences in infancy, and the relative extent of genetic and environmental influence varies for different characters. We have no doubt that these general principles hold for early childhood as well as for infancy.
One other general principle should be added to our earlier list: Individual differences among children are substantial and reliable.
For the last twenty years considerable interest has been directed towards brain research. One of the main reasons for this is the concentration by medical researchers on particular organs with the aims of understanding the total functioning of such organs and of investigating the possibility of their replacement by younger and more efficient units. Kidney and heart transplantation are now practised widely and there has been some success in overcoming initial difficulties caused by organ rejection. One problem is whether the experience gained with these organs could be applied to the central organ, the brain. Let us first consider the technical aspects. The multiple nervous connections that carry sensory input to the brain and outgoing commands to the periphery, the cranial nerves, mean that neural reconnection is biologically and technically impossible (for reasons discussed later). A second problem would be the rejoining of blood vessels. Microsurgery would make this technically feasible, but the brain's continuous need for oxygen would hardly allow sufficient time for transplantation, even if the replacement brain were cooled. But the real problem lies elsewhere. The brain represents the signature of a genetically unique person: the individual fate and memories of that particular person, his or her character. In short, the existence of individual life history makes the idea of a cerebral replacement a foolish and worthless concept.
The idea of brain transplants apart, research on brain structure and function has made great leaps forward since the development of methods for analysing morphological and functional aspects of the brain. Comparative biology and evolutionary principles soon showed that the human brain shared common features with the brains of all vertebrates.
One reason for the relative disregard of individual differences in psychology is that research on this subject appears atheoretical and usually addresses correlation rather than causation. In this chapter, we suggest that quantitative genetics provides the basis for a general theory of the etiology of individual differences of scope and power rarely seen in the behavioral sciences. After a brief overview of quantitative genetics, we describe a general theory of individual differences in terms of 10 propositions and then consider the theory in the context of current trends in the philosophy of science.
We will not concern ourselves with the philosophical intricacies of the word “theory.” The term obviously means different things to different psychologists, as illustrated by formal differences among the best-known theories in psychology, such as learning theories, personality theories, and Piagetian theory. Nonetheless, from the pragmatic view of a behavioral researcher, theories should clarify our thinking by describing, predicting, and explaining behavior. At the very least, theories should be descriptive, organizing and condensing existing facts in a reasonable, internally consistent manner. However, they should also make predictions concerning phenomena not yet investigated and allow clear tests of these predictions to be made. At their best, theories explain phenomena as well as describe and predict them.
The ability to smell, a highly sensitive modality even in Man, is of great significance for our social life, both physiologically and psychologically. From a biochemical point of view olfaction is related to taste and both are chemical senses. Many animals are guided almost exclusively by the sense of smell in periods of sexual activity, and dogs and cats appear almost blind and deaf to other stimuli when ‘on heat’. A surprisingly small amount of substance is required for detection by olfactory receptors.
To characterise the strong effect odours have on behaviour a specific term ‘pheromone’, was introduced by Karlson & Lüscher (1959) in their work on insects searching for a mate and guided by odour. Pheromones are olfactorily active substances which, when smelled, trigger a specific behavioural pattern in neuroendocrine mechanisms in a similar way to hormones. These pheromones may cause profound changes in endocrine secretory systems or may simply attract the opposite sex, in which case they are referred to as primer pheromones (Keverne, 1983).
The sense of smell in Man is highly efficient, in spite of the fact that the area in the nose housing the receptors is very small (Figs 9.35 and 11.1) and the greater part of our nasal mucosa serves to warm the inhaled air. The olfactory cells in Man occupy a relatively small area in the upper part of the nose and nasal septum and, for this reason, odiferous substances transported by air and inhaled do not reach this upper nasal portion (Fig. 9.35) directly but by diffusion inside the nose. This is why we sniff the air in order to reach the receptors.
Genotype–environment interaction, the topic of the preceding chapter, denotes an interaction in the statistical, analysis-of-variance sense of a conditional relationship: The effect of environmental factors depends on genotype. In contrast, genotype–environment correlation literally refers to a correlation between genetic deviations and environmental deviations as they affect a particular trait. In terms of a 2 × 2 table depicting low versus high genotypes reared in low versus high environments, evidence for genotype–environment interaction is obtained from a comparison of cell means (e.g., cells 1 and 4 vs. cells 2 and 3). In contrast, genotype–environment correlation is indicated by the frequency of individuals in the cells (e.g., more children of “high genotype” are likely to experience the “high environment”). In other words, genotype–environment correlation describes the extent to which children are exposed to environments on the basis of their genetic propensities. For example, if shyness is heritable, children genetically predisposed toward shyness will have shy parents on the average who are likely to provide a “shy” environment for their children – that is, modeling shy behavior and providing relatively few opportunities for interactions with strangers. Such proclivities can be reinforced in interactions with nonfamily members: Reactions of unfamiliar children and adults to a shy child are unlikely to be rewarding or successful for the child, thus enhancing the child's tendencies toward shyness.
The full adoption design allows us to investigate the etiology of individual differences in behavior in a direct and straightforward manner. The design is both simple and powerful, and the summary statistics it yields provide a broad description of this etiology, as we have seen in the preceding chapter. The correlation between the behavior of the adopted child and that of its adoptive parents provides direct evidence of the importance of shared environment independent of inherited, or genetic, influences. The correlation between the behavior of the adopted child and that of the biological parents from whom the child has been separated since birth provides direct evidence of the importance of genetic influences independent of the home environment. In nonadoptive families these two influences are always confounded and there is no direct way to evaluate their relative importance.
Simple correlations estimated from adoption data provide a very broad description that, for many purposes, may be quite sufficient for an understanding of the etiology of individual differences. Alternatively, a model of transmission may be assumed that facilitates estimates of genetic and environmental transmission parameters. The adoptive-parent/adopted-child correlation provides an estimate of the proportion of variance due to shared environmental influences (c2), whereas the biological-parent/adopted-child correlation estimates one-half of heritability (h2).
The bioelectric current– basis for signal transmission
As living cells are unable to utilise a metallic conductor for communication, they have chosen other means: (1) extracellular for fluid metabolic products; (2) vascular transport for hormones; and (3) ionic generation of propagated membrane potentials. Cells can accumulate negatively charged molecules inside as a result of having a selectively permeable outer membrane. Thus, a potential difference exists between the cell's interior and the outside medium, and can be used for processes of de- and repolarisation. Electrical transmission of signals by the nervous system was investigated in the first half of the nineteenth century by eminent physiologists such as Dubois-Reymond (1843) and later by Hermann (1883) and Bernstein (1902). Galvani and Volta in Italy had already recognised the presence of electric currents in frog muscle, although Volta believed that the muscle only produced a current when metals were in contact with the moisture and salt of the muscle, rather like a battery. Galvani's work was carried on by Valli and eventually it was commonly agreed that the resting muscle had an electrical potential difference across it, with a negative charge within the muscle and a positive charge on its outside. The presence of a potential difference across an inactive muscle (the resting potential) was well demonstrated by the actual flow of current which was released when the muscle was injured. Nobili (1825) for instance, recorded a marked flow of current in a frog muscle preparation, which he, not unnaturally, called the ‘frog current’.
Infancy blossoms into childhood with the dramatic changes of the second and third years of life. These average changes from infancy to early childhood are so marked that one of the founders of developmental psychology, James Mark Baldwin (1894), suggested that, during the first year, infants possess only the properties of lower vertebrates; during the second year, they employ processes of higher vertebrates; not until the third year of life, however, do children begin to use cognitive processes characteristic of the human species. Although Baldwin's ontogeny-recapitulates-phylogeny interpretation of the changes from infancy to early childhood would find few adherents today, no one would deny that the average changes from infancy to early childhood are considerable. It is critical, however, to recognize that what we know about the transition from infancy to early childhood is limited primarily to average age differences rather than to individual differences.
This chapter discusses what is meant by developmental change in terms of individual differences rather than average age differences. Developmental change in terms of individual differences can be quite different from normative change because, as discussed in Chapter 2, the description and explanation of group differences are not necessarily related to individual differences. Indeed, it has been suggested that “there may be an inverse relationship between the suitability of a dimension as an expression of individual differences and its status as a dimension of major developmental change” (Wohlwill, 1973, p. 335).
Everything psychologists measure in the family environment is at least indirectly a measure of parental behavior. This is obvious for the two “superfactors” parental warmth and control, but it is just as true for physical aspects of the home environment such as number of books in the home. Consider, for example, the most widely used measure of the family environment, Caldwell and Bradley's (1978) Home Observation for Measurement of the Environment (HOME). Each of the 45 items clearly involves parental behavior; for example, the first item is “mother spontaneously vocalizes to child at least twice during visit.” The six scales of the HOME also indicate the behavioral nature of the HOME: emotional and verbal responsivity of the mother, avoidance of restriction and punishment, organization of the physical and temporal environment, provision of appropriate play materials, maternal involvement with child, and opportunities for variety in daily stimulation.
If measures of the home environment are viewed as indirectly assessing parental behavior, variations in such parenting measures can be studied from a quantitative genetic perspective. This perspective leads us to investigate the etiology of differences in childrearing behavior among parents and to consider genetic as well as environmental components of variance. Genetic variance can lead to variability on a measure of parenting for two reasons.
Teaching in Cambridge proved to be refreshing and stimulated my wish to write a new version of my earlier book, Das menschliche Gehirn (Hippokrates Verlag Stuttgart, 1968), drawing upon my experience and accumulated teaching material. This new book attempts, as did an earlier one (Experimental Neurology, Clarendon Press, Oxford, 1961), a combination of morphological data with physiological and neurological studies.
Being primarily a morphologist rooted in the concept of the evolution of structure I have placed the emphasis on structural organisation, but functional aspects, experimental research and clinical findings have been incorporated, broadening the interest for clinical students and for students of neurobiology.
I wish to thank Professor R. J. Harrison, FRS for his offer of a base in his department from which I could take part in departmental teaching and continue my research, supported by the Deutsche Forschungsgemeinschaft; and Dr J. Herbert, Fellow of Gonville and Caius College, and Professor W. J. Macpherson, President of the College, for making mean Associate Member of the College, enabling me to teach some of their medical students. I also wish to thank students from Gonville and Caius College, in particular Pak-Lee Chau, David Evans, Diane Hopper, John Williams and Kwong-Wai Man for their help in various ways. My thanks to Petra Schuba for her great illustrative skill, to Mrs F. Glees for her secretarial help, to Tim Crane and Dennis McBrearty for their expert technical assistance and to Herr G. Koch, Gesellschaf t für wissenschaftliche Datenverarbeitung, Göttingen, for help with the index. I am indebted to the staff of Cambridge University Press, for their patience and linguistic support during the preparation of this book.
The goal of this book is to explore the origins of individual differences in behavioral development during infancy and early childhood. A key phrase is “individual differences.” When developmentalists look at infancy and early childhood, they are usually absorbed by the dramatic changes that members of our species undergo during this fast-moving period of development. For example, Jean Piaget, the most influential figure in developmental psychology since the 1960s, described cognitive changes in terms of the transition from the sensorimotor actions of infancy to the representational abilities of early childhood, seen most clearly in the blossoming of language. However, Piaget was concerned only with average developmental trends, not with differences among children.
In contrast, when we look at children, we see children, not the child. That is, our interest centers on the development of individual differences among children rather than universal or normative (average) aspects of our species' development. A powerful theory of development must be able to explain individual differences, if for no other reason than that such differences exist – individual differences represent a major part of the phenomenon to be explained. There are, however, other reasons for studying individual differences: Descriptions and explanations of normative aspects of development bear no necessary relationship to those of individual differences; questions concerning the origins of individual differences are more easily answered than questions concerning the etiology of normative aspects of development; and the developmental issues of greatest relevance to society are issues of individual differences.