Nature and Nurture in Personality

Despite high initial expectancy, studies of behavioral genetics have not provided satisfactory results in personality psychology. The failure to identify the specific genetic underpinnings of behavior could be related to its multifactorial nature and the lack of biological validity of the personality concept and the important influence of the environmental factors on personality. A promising way to solve this problem is to look at the early biological roots of personality. Here, research has been concentrated on temperament, because an understanding of neuroregulatory systems underlying temperament may increase our knowledge of the interplay of nature and nurture in a development of normal personality and, in particular, may highlight mechanisms through which unfavorable and adverse environmental effects turn into personality disorders (7).

Temperament consists of those components of personality that are heritable, developmentally stable, emotion based, or uninfluenced by sociocultural learning (8). Recent literature offers extensive evidence to show that interindividual differences in neuroregulatory systems, especially in the activities of the brain dopamine and serotonin systems, explain temperamental variability. This suggestion was originally made by Cloninger in his temperament and character theory (9). Cloninger conceptualizes personality as the combination of heritable, neurobiologically based temperament traits reflecting behavioral conditioning, and character traits reflecting both neurobiological and sociocultural mechanisms of semantic and self-aware learning. According to him, temperamental dimensions are related to heritable variation in responses to environmental stimuli and characterized by novelty seeking (NS) (a tendency toward exploratory activity and intense excitement in response to novel stimuli), harm avoidance (HA) (a tendency to respond intensely to aversive stimuli and to avoid punishment and novelty), and reward dependence (RD) (a tendency to respond intensely to reward and to learn to maintain rewarded behavior). NS is suggested to be linked with low basal dopaminergic activity, HA with high serotonergic activity, and RD with low basal noradrenergic activity (9). The extreme variants of these basic stimulus-response characteristics closely correspond to the traditional descriptions of personality disorders. This correspondence implies that the underlying structure of the normal adaptive traits is basically the same as that of the maladaptive personality traits.

The molecular genetics of temperament started in 1996 with two articles (10, 11) that showed an association between NS and the dopamine 4 receptor (DRD4). This finding was shortly replicated in many studies (12, 13), although some further studies questioned this association (14, 15). These two first articles on NS were shortly followed by investigations linking HA with the allelic variation of the serotonergic genes, first with the serotonin transporter 5HTTLPR. This link was also replicated (16, 17), even though the number of inconsistent findings was high (18).

In the 2000s, single gene effects as well as coeffects of several genes on temperament were increasingly documented, whereas studies using traditional personality traits were few in number. Gene × environment interactions in the development of temperament and personality have received less attention. The first molecular gene × environment interaction studies of human behavior were carried out by Berman and Noble (19) and Ozkaragoz and Noble (20), who showed that in adolescent boys, the minor alleles of the DRD2 gene interacted with familial alcoholism, resulting in high extraversion.

Later, it was demonstrated that the 5HTTLPR gene moderates parental influences on early temperament development. It has been shown that infants carrying the short allele of 5HTTLPR developed poorer behavioral self-regulation than their counterparts carrying only long alleles if they were insecurely attached to their caregivers but not when they were securely attached (21). Likewise, Fox et al. (22) showed that the short allele increased behavioral inhibition in children who had low parental support.

Our series of studies has capitalized on the population-based, longitudinal birth cohort study of the Cardiovascular Risk in Young Finns (Table 1). In this study, a representative sample of 3,600 healthy subjects from six age cohorts (aged 3, 6, 9, 12, 15, and 18 years at the baseline) have been followed over 27 years since their childhood and monitored in eight study waves resulting in a huge reservoir of somatic, psychological, behavioral, and environmental predictors and somatic and psychological outcomes (23) (Figure 1).

Together with other studies of gene-environment interactions, our series of studies suggest that depending on their genotype, people may be differentially sensitive to the environmental conditions they encounter. In addition, it seems that a certain genetic background may sensitize a person both to the positive and the negative aspects of the environment suggesting that a gene variant may not be acting solely as a “vulnerability factor” nor a pure “opportunity gene” that would be entirely good or bad for its carrier (44). For example, the allelic variance of the HTR2A gene was shown to be associated with both an ability to use positive aspects of the environment, when offered, and with a heightened vulnerability to negative aspects of the environment, this way affecting the overall responsivity to environmental conditions. In addition to current environmental effects, certain gene variants may influence the duration of early experiences. In light of these results it seems highly plausible that the effects of genes may become evident only when studied in the context of environmental factors, whereas ignoring environmental variability may lead to inconsistent replications of findings, as has often been observed for multifactorial traits.

It is known that any extreme temperamental bias may predispose a person to personality disorders (45). Genetic background not only delineates early temperament but also determines how malleable these dispositions are in response to the environment. In some individuals, high anxiousness (which is strongly correlated with HA) may be the result of genetics and insensitivity to environmental influences that would decrease anxiousness in more sensitive individuals. In others, high anxiousness may reflect a combination of high susceptibility and exposure to environmental influences increasing anxiousness. The study of gene-environment interactions helps us to understand the origins and consequences of temperament and personality traits that stem from these different developmental pathways.

Despite high consistency of the findings on the joint effect of genes and environment, one weakness needs to be recognized. This weakness limits our findings as well as most previous research. “Environment” usually refers to parental parameters that at least partly indicate a shared genetic background, too. Thus, the environment may be partly genetic. Nevertheless, adoption studies and other separation experiments indicate that both nature and nurture need to be considered carefully in assessing the development of temperament, personality, and their disorders. Neither genes nor environmental influences alone can be expected to explain the development of personality across the lifespan.