review below, more recent evidence challenges some of the standard interpreta-tions of this research; see Diener, Lucas, & Scollon, 2006). Second, well-being is heritable and can be linked to psychophysiological structures and processes.
Third, as noted well-being scores are quite stable over time, even in the face of major life changes. And finally (and perhaps most directly), well-being scores are often moderately to strongly correlated with stable personality traits. Because the first of these four pieces of evidence (the small role of external circumstances) has been addressed in quite a bit of detail elsewhere (e.g., Argyle, 1999; Diener et al., 1999), and because it is only indirectly related to the topic of personality and well-being, I focus mostly on the remaining three pieces of evidence.
compo-nents. If the effects of genes on subjective well-being are additive, then the more genes that two people share, the more similar they should be. Nonadditive genetic effects, on the other hand, reflect interactions among genes. In the extreme case, two people would need the exact same combination of genes to express the same phenotype. Thus, two people who were genetically related but not genetically identical could end up being no more similar than average, even if the trait in question were 100% heritable. Nonadditive effects are suggested when monozygotic twin correlations are more than twice as high as dizygotic twin correlations. Tellegen et al. found that the effects of negative emotionality were completely additive, whereas the effects of positive emotionality were com-pletely nonadditive.
Researchers have attempted to replicate and extend Tellegen et al.’s (1988) study several times using a variety of techniques and measures. In general, the estimated contribution of broad heritability versus shared environment has held up quite well. For instance, Roysamb, Harris, Magnus, Vitterso, and Tambs (2002) examined the heritability of subjective being using a global well-being measure, and like Tellegen et al., they found that about 50% of the vari-ance could be accounted for by genes. Again, models that included shared envi-ronmental factors did not fit significantly better than models without these fac-tors.
Interestingly, Roysamb et al. (2002) found that the heritability of well-being differed across sexes. Heritability was estimated at .54 among women and .46 among men (also see Roysamb, Tambs, Reichborn-Kjennerud, Neale, & Harris, 2003, for a replication with a larger but overlapping sample). Perhaps more importantly, because Roysamb et al. included both same-sex and mixed-sex fra-ternal twins, they could estimate whether the same genes contributed to the hap-piness of men and women. If so, the correlations among same-sex dizygotic twins should be the same size as the correlations among the mixed-sex dizygotic twins. This was not the case, and Roysamb et al. estimated that the correlation between the genetic effect in men and the genetic effect in women was just .64.
The authors explained this effect in terms of potential underlying mechanisms. It is possible that there is a direct temperamental effect on well-being, and that this effect is explained by the same genes across sexes. However, there may also be indirect effects, whereby genes lead individuals to select certain environments, and these environments lead to individual differences in happiness. The specific environments that promote happiness may differ for men and women. Roysamb et al. argued that the fact that the genetic effects for men and women are not per-fectly correlated suggest that at least part of the effect of genes is indirect.
Because subjective well-being includes a variety of separable components that may result from different processes, it is possible that heritability may vary for the distinct components. Tellegen et al. (1988) examined the heritability of vari-ous facets and factors from the MPQ (which was intended as a measure of stable
personality), and Roysamb et al. (2002) used a three-item well-being measure that incorporated questions about all three major components of subjective well-being: positive affect, negative affect, and life satisfaction. Other researchers have attempted to determine the heritability of other components, including short-term mood or long-short-term levels of life satisfaction. For example, Stubbe, Posthuma, Boomsma, and De Geus (2005) examined the heritability of life satis-faction using the Satissatis-faction with Life Scale (Diener, Emmons, Larsen, & Grif-fin, 1985) in a sample of over 5,000 twins from The Netherlands. Their analyses suggested that 38% of the variability in life satisfaction is heritable—a finding that is slightly lower than the estimates from Tellegen et al. or Roysamb et al. Fur-thermore, they estimated that almost all of these genetic effects were nonadditive.
In direct contrast to the results of Roysamb et al., Stubbe et al. found that the correlation between dizygotic same-sex twins was not significantly different from the correlation between mixed-sex twins or even siblings. Although they did not model these differences in the same way that Roysamb et al. did, this pattern of correlations contradicts Roysamb et al.’s finding that the correlation among men’s and women’s genetic factors is substantially less than 1.
In one of the most novel behavioral–genetic studies on the heritability of well-being, Riemann, Angleitner, Borkenau, and Eid (1998) assessed mono-zygotic and dimono-zygotic twins’ moods across five different mood-induction condi-tions. Thus, in contrast to the other behavioral–genetic studies, the focus was on short-term moods rather than on long-term affective traits. Interestingly, Riemann et al. reported results that differed quite a bit from the studies reviewed above. Even when average mood levels across all five situations (which, theoreti-cally, should be highly correlated with affective traits) were examined, estimated heritabilities were much lower than those found in previous studies. Heritabilities ranged from .18 to .19 for negative mood and from .11 to .16 for positive mood.
In addition, unlike previous studies, the shared environmental component accounted for at least as much, and sometimes more, variance than did genes.
The shared environment accounted for between 31 and 32% of the variance in negative mood and between 15 and 18% of positive mood. Because behavioral–
genetic researchers have grown accustomed to finding moderate heritabilities and almost no shared environment for just about any personality characteristic that is examined (Turkheimer, 2000), Riemann et al.’s results are quite surprising.
Perhaps the most controversial study on the heritability of well-being is Lykken and Tellegen’s (1996) paper entitled “Happiness Is a Stochastic Phenom-enon.” In it, the authors used a longitudinal study of twins to determine the extent to which the stable component of well-being is heritable. They found that over a 10-year period, the stability of well-being was about .50. However, the cross-twin, cross-time correlation (i.e., twin 1’s time 1 score correlated with twin 2’s time 2 score) was .40. Because this cross-twin, cross-time correlation is 80%
as large as the stability coefficient, Lykken and Tellegen estimated that 80% of the
stable component of well-being is heritable. The authors suggested that this extremely high heritability means that “trying to be happier [may be] as futile as trying to be taller” (p. 189).
However, there are a number of problems with this conclusion. First, as Lykken himself noted (Lykken & Csikszentmihalyi, 2001), even in the twin study he analyzed, only about 50% of the variance was stable over a 10-year period. Thus, even if Lykken and Tellegen’s (1996) estimates are correct, then it is more accurate to say that trying to change the part of our happiness that does not change is like trying to be taller (which, of course, is tautological). However, even this qualified statement may not be completely accurate. Strong heritability on its own does not necessarily mean that something cannot be changed. Because genes may lead to happiness indirectly (e.g., through choice of environment or exposure to life events), it is possible that change can be achieved once the underlying process is understood.
Furthermore, it is important to remember that Lykken and Tellegen’s (1996) conclusion is based on one study with a relatively small sample of twins (79 monozygotic twin pairs and 48 dizygotic twin pairs). Although the broad heritability of well-being has been replicated often, many of the extensions of these findings have not replicated well. And there is some reason for concern about the reliability of the estimates from this small sample. Although it is not reported in the Lykken and Tellegen paper, the time 2 correlation between monozygotic twins was only .13 (compared to a time 1 correlation of .63, and a time 2 correlation between dizygotic twins of .23; McGue, Bacon, & Lykken, 1993). The time 2 pattern of monozygotic and dizygotic correlations would actually suggest no genetic effect and a small shared environmental effect on well-being—a finding that contradicts a fairly large body of research.
Furthermore, two more recent studies have reached different conclusions about the heritability of the stable component of well-being. Although Nes, Roysamb, Tambs, Harris, and Reichborn-Kjennerud (2006) replicated Lykken and Tellegen’s estimates, Johnson, McGue, and Krueger (2005) found that only about 38% of the stable variance in well-being is heritable. Thus, additional repli-cations are needed before researchers can accept the estimates from Lykken and Tellegen’s study.
Overall, behavioral–genetic studies have repeatedly shown that happiness is heritable. Genes appear to account for about 40–50% of the variance in stable levels of positive affect, negative affect, life satisfaction, and other aspects of global well-being. At this point, it is unclear whether these genetic effects are additive or nonadditive, and it is unclear whether there are any reliable shared family environmental effects (though, as with most personality traits, the answer is probably “no”). Furthermore, the genes that underlie these effects may or may not vary for men and women. And finally, some evidence suggests that heritabilities are lower for state levels of mood—even when these measures are
aggregated over multiple occasions—and higher for long-term levels of well-being. Taken together, the behavioral–genetic studies suggest that inborn biol-ogy plays at least some part in determining happiness.
Specific Psychophysiological Correlates
Behavioral–genetic studies show that at least some portion of the variance in well-being can be explained by genes. And, of course, genes must express them-selves through some physiological process. However, the exact mechanisms by which these genetic effects are transmitted are not known. It is possible that the genetic effects are direct. Specific genes or combinations of genes may influence average hedonic tone, emotional reactivity, or emotional intensity. Alternatively, the genetic effect may be indirect. Genes may influence physiological systems that only indirectly influence well-being through their effects on environmental choice or other behaviors. Thus, behavioral–genetic studies alone cannot deter-mine how genes and biology influence well-being. More targeted studies that examine the specific psychophysiological systems that may be involved in affec-tive experience are required.
Perhaps the most studied neural correlate of self-reported well-being is asymmetrical hemispheric activation in the prefrontal cortex (for a review, see Davidson, 2004). For decades, Davidson and colleagues (and others) have inves-tigated whether greater left versus right hemispheric activity is associated with approach-oriented emotions (e.g., happiness and excitement), and greater right versus left activity is associated with withdrawal-oriented emotions (e.g., fear and disgust). For instance, Davidson et al. (1990) measured brain activity during films designed to induce happiness or disgust. In accordance with their hypotheses, the happy films were associated with greater left versus right frontal and anterior temporal activity, whereas the disgust films were associated with greater right versus left activity. Thus, at a state level, this psychophysiological measure has been shown to correlate with positive versus negative emotion.
Perhaps more importantly for researchers interested in individual differences in subjective well-being, there appear to be stable individual differences in hemi-spheric asymmetry. For instance, Tomarken, Davidson, Wheeler, and Kinney (1992) took multiple assessments of baseline electrical activity within two occa-sions separated by 3 weeks. Internal consistency (calculated using multiple trials within a single session) was very high (α> .85) and test–retest reliabilities were similar to short-term test–retest reliabilities for standard self-report measures of subjective well-being (they ranged from .65 to .75). Thus, there appear to be sta-ble individual differences in asymmetrical activity.
These individual differences in hemispheric asymmetry have been shown to correlate with well-being. For example, Tomarken, Davidson, Wheeler, and Doss (1992) showed that individuals with relatively high left frontal activation
reported more positive affect and less negative affect than individuals with rela-tively high right frontal activation. More recently, Urry et al. (2004) extended these results to measures of well-being beyond positive and negative affect. They showed that even measures of psychological well-being (which include scales for such constructs as self-acceptance, purpose in life, personal growth, and auton-omy) were predicted by prefrontal asymmetry. Davidson and Fox (1989) showed that even among 10-month-old infants, asymmetry in prefrontal activation pre-dicted distress in response to maternal separation. These results are also consistent with earlier studies showing that damage to the left prefrontal cortex is more likely to lead to depressive symptoms than is damage to the right prefrontal cor-tex (see Davidson, 2004, for a review).
Davidson and colleagues have also used additional techniques to determine exactly how these psychophysiological differences are related to subjective well-being. They believe that asymmetry does not directly influence average hedonic tone. Instead, it is thought to be a diathesis that predicts various aspects of the response to emotional challenge. For instance, in one study, Wheeler, Davidson, and Tomarken (1993) showed that baseline measures of asymmetry predicted reaction to emotional films. Greater left prefrontal activation was associated with more intense positive affect after a positive film; greater right prefrontal activa-tion was associated with more intense negative affect after a negative film.
Larson, Sutton, and Davidson (1998) showed that asymmetry may be related to emotion regulation. This group of researchers took advantage of the fact that negative emotions potentiate the startle response. By assessing this startle response at varying intervals after the presentation of a negative stimulus, they could deter-mine how long the potentiating effects of the negative mood lasted. Larson et al.
found that prefrontal asymmetry was unrelated to the magnitude of the startle response during the presentation of the stimulus, but this measure did predict startle magnitude after the offset of the stimulus. The authors interpreted this effect to mean that prefrontal asymmetry is associated with automatic recovery (a form of emotion regulation) after the emotional event.
Although much of the research that focuses explicitly on the psychophysio-logical underpinnings of subjective well-being has centered on hemispheric asymmetry, research in other domains is also relevant. For instance, LeDoux and colleagues (see LeDoux, 2000, and LeDoux & Phelps, 2000, for reviews) have amassed a large body of evidence showing that the amygdala is involved in emo-tional processing. The amygdala appears to be involved in the conditioning of fear, and LeDoux and Phelps suggested that “the amygdala plays an important role in the assignment of affective significance to sensory events” (p. 158). It is still unclear whether and how individual differences in amygdalar activity are related to subjective well-being, though Abercrombie et al. (1998) provided evi-dence that metabolic rate in the right amygdala does predict negative affect. Fur-thermore, Canli et al. (2001) were able to show that greater activation to positive
relative to negative pictures in the right amygdala was associated with scores on an extraversion measures. According to the authors, this finding was the first demonstration that the amygdala—which is usually associated with the process-ing of negative information—is also involved in the processprocess-ing of positive stim-uli.
Other theories focus on general systems that may underlie broad, affective and motivational traits (e.g., Cloninger, 2004; Gray, 1970). For instance, within the context of affiliative behavior, Depue and his colleagues (Depue & Collins, 1999; Depue & Morrone-Strupinsky, 2005) have linked a variety of psy-chophysiological processes with emotions. Specifically, Depue and Morrone-Strupinsky suggested that affiliative behavior could be broken down into two distinct phases of activity, both of which are intimately involved with psycho-physiologically based emotional processes. In an appetitive phase of affiliative behavior, dopamine systems affect the feelings of excitement as an organism approaches a potential reward. In a consummatory phase, opiate systems affect feelings of pleasure, gratification, and liking that result from the attainment of a social reward. Although Depue and Morrone-Strupinsky link individual differ-ences in these systems to the personality trait of affiliation, the processes involved have clear relevance for well-being. Differential functioning in these systems may result in individual differences in the emotions that ultimately promote affiliative behavior.
It is tempting to conclude from this research that differences in these psychophysiological processes provide the link from genes to the observed indi-vidual differences in well-being. It is also tempting to infer that because these underlying differences are biologically based, they are difficult, if not impossible, to change. However, Davidson (2004) is careful to point out that such a conclu-sion would be premature. For instance, animal studies have shown that early environment can directly affect the biological systems that govern emotional response to stressors (e.g., Francis & Meaney, 1999). Furthermore, Davidson and colleagues have shown that some of the physiological indicators that have been linked with subjective well-being can change over time. For instance, an 8-week mindfulness meditation training program led to changes in asymmetry that mir-ror the individual differences described above (Davidson et al., 2003). Thus, it is important not to infer from these biological differences that subjective well-being cannot change.