It is reasonable to expect that descriptive and explanatory relationships in development involve complex interactions rather than simple main effects. For example, an easy temperament might buffer a child against a difficult environment; conversely, stress may have a disproportionate effect on vulnerable children (Garmezy & Rutter, 1983). Organismic specificity in reaction to environments is one of the major hypotheses that emerges from a thorough review of early experience and human development:

Both from basic and applied data it has become increasingly clear that the relationship of early experience to development will be mediated by the nature of the organism on which the experience impinges. Unfortunately, virtually nothing is known about the specific organismic characteristics which mediate differential reactivity to the early environment. (Wachs & Gruen, 1982, p. 247)

In this chapter, we explore interactions using the CAP data in early childhood. The word “interaction” has many connotations, and it is important to be clear about its use. We limit our search for interactions to statistical interactions, the type of interaction typically derived in analysis of variance that involves the sum of squares remaining after main effects and within-cell variation is removed: “The phenomenon is well named. Interaction variations are those attributable not to either of two influences acting alone but to joint effects of the two acting together” (Guilford & Fruchter, 1973, p. 249).

Behavioral genetic theory, methods, and research provide a unique perspective on nature and nurture during infancy and early childhood, that is, on the genetic and environmental origins of individual differences in behavioral development. The words “nature” and “nurture” each have warm associations until they are brought together. One of our goals is to emphasize the conjunction “and” rather than the projective test provided by the dash in “nature–nurture” or the explicit hostility in the phrase “nature versus nurture.” We believe that the perspective of behavioral genetics is as useful for understanding environmental influences in development as it is for exploring the role of heredity, and we hope that this book will convince developmentalists of the importance of both genetic and experiential factors in the origins of behavioral differences during infancy and early childhood. At the simplest level, the components-of-variance approach – which we explore in terms of simple correlations as well as by means of model-fitting analyses – often indicates that genetic variance is significant and invariably shows that nongenetic factors are important.

The decomposition of phenotypic variance into genetic and environmental components of variance is the standard fare of behavioral genetic research. Somewhat newer is an emphasis on the decomposition of the environmental component of variance into two components, one shared by family members, which increases their phenotypic resemblance, and the other not shared; correlations for genetically unrelated children reared together in the same adoptive homes are especially powerful for detecting the “bottom line” influence of growing up in the same family.

Interest in as well as understanding and acceptance of behavioral genetics are often hindered by a single issue: confusion between individual differences and group differences. That is, behavioral genetic theory and research address individual differences (variance), whereas most psychological research involves group comparisons (means). In this chapter, we contrast these two approaches and then discuss the advantages and disadvantages of an individual-differences perspective. In part, the relative neglect of an individual-differences approach is due to its apparent atheoretical orientation. For this reason, the next chapter considers quantitative genetics as the basis for a general theory of the origins of individual differences.

The group-differences approach focuses on average differences, such as gender, age, cultural, or species differences, among groups of individuals within a population. In contrast, the etiology of differences among individuals in a population is the focus of individual-differences research. The point of this chapter is not that the individual-differences approach is better than the group-differences approach. The two approaches are perspectives, and perspectives are neither right nor wrong, only more or less useful for a particular purpose. However, we do argue that the two approaches differ in important ways that affect theories and research. In the following section, the basic distinction between the two approaches is examined more closely.

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.

Olfaction

Introduction

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’.