Type of Project
Abstract Behavior genetics has demonstrated that genetic variance is an important component of variation for all behavioral out- comes, but variation among families is not. These results have led some critics of behav- ior genetics to conclude that heritability is so ubiquitous as to have few consequences for scientific understanding of development, while some be- havior genetic partisans have concluded that family environ- ment is not an important cause of developmental outcomes.
Both views are incorrect. Geno- type is in fact a more system- atic source of variability than environment, but for reasons that are methodological rather than substantive. Development is fundamentally nonlinear, interactive, and difficult to con- trol experimentally. Twin stud- ies offer a useful methodologi- cal shortcut, but do not show that genes are more fundamen- tal than environments.
Keywords genes; environment; develop- ment; behavior genetics
The nature-nurture debate is over. The bottom line is that every- thing is heritable, an outcome that has taken all sides of the nature- nurture debate by surprise. Irving Gottesman and I have suggested that the universal influence of genes on behavior be enshrined as the first law of behavior genetics (Turkheimer & Gottesman, 1991), and at the risk of naming laws that I can take no credit for discovering, it is worth stating the nearly unani- mous results of behavior genetics in a more formal manner.
c First Law. All human behavioral traits are heritable.
c Second Law. The effect of being raised in the same family is smaller than the effect of genes.
c Third Law. A substantial portion of the variation in complex hu- man behavioral traits is not ac- counted for by the effects of genes or families.
It is not my purpose in this brief article to defend these three laws against the many exceptions that might be claimed. The point is that now that the empirical facts are in and no longer a matter of serious controversy, it is time to turn atten- tion to what the three laws mean,
to the implications of the genetics of behavior for an understanding of complex human behavior and its development.
VARIANCE AND CAUSATION IN BEHAVIORAL
If the first two laws are taken literally, they seem to herald a great victory for the nature side of the old debate: Genes matter, families do not. To understand why such views are at best an oversimplifica- tion of a complex reality, it is nec- essary to consider the newest wave of opposition that behavior genet- ics has generated.
These new crit- ics, whose most articulate spokes- man is Gilbert Gottlieb (1991, 1992, 1995), claim that the goal of devel- opmental psychology is to specify the actual developmental processes that lead to complex outcomes. In lower animals, whose breeding and environment can be brought under the control of the scientist, it is possible to document such devel- opmental processes in exquisite detail.
The critics draw an unfavor- able comparison between these detailed animal studies and twin studies of behavior genetics, which produce only statistical conclu- sions about the relative importance of genes and environment in devel- opment.
The greatest virtue of the new challenge is that it abandons the
Three Laws of Behavior Genetics and What They Mean Eric Turkheimer1 Department of Psychology, University of Virginia, Charlottesville, Virginia
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implausible environmentalist con- tention that important aspects of behavior will be without genetic influence. Gottlieb (1992) stated, “The present . . . viewpoint holds that genes are an inextricable com- ponent of any developmental sys- tem, and thus genes are involved in all traits” (p. 147). Unlike earlier critics who deplored the reduction- ism they attributed to behavior genetic theories of behavior, the developmental biologists take be- havior genetics to task for not be- ing mechanistic enough.
Once vili- fied as the paragon of determinist accounts of human behavior, be- havior genetics is now chastised for offering vague and inconclusive models of development (Gottlieb, 1995; Turkheimer, Goldsmith, & Gottesman, 1995), and judged by the standards of developmental psychobiology in lower animals, it is true enough that behavior ge- netic theories of complex human behavior seem woefully poorly specified.
But ultimately the charge is unfair, because there is no equivalent in developmental psy- chobiology to the behavior genetic study of marital status or school performance. The great preponder- ance of the exquisite experimental science that goes into animal psy- chobiology is quite simply impos- sible to conduct in humans.
Human developmental social science is difficult equally so for the genetically and environmen- tally inclined because of the (methodologically vexing, human- istically pleasing) confluence of t w o c o n d i t i o n s : ( a ) B e h a v i o r emerges out of complex, nonlinear developmental processes, and (b) ethical considerations prevent us from bringing most human developmental processes under effec- tive experimental control.
Figure 1 is a schematic illustration of the problem. Individual genes (Genes 1, 2, and 3) and their environments (which include other genes) inter- act to initiate a complex develop- mental process that determines adult personality. Most characteris- tic of this process is its interactivity.
Subsequent environments to which the organism is exposed depend on its earlier states, and each new en- vironment changes the develop- mental trajectory, which affects fu- ture expression of genes, and so forth. Everything is interactive, in the sense that no arrows proceed uninterrupted from cause to effect; any individual gene or environ- mental event produces an effect only by interacting with other genes and environments.
For the behavior geneticist,
Fig. 1. Schematic diagram of contrasting roles of genes and environment in development of personality. One-headed arrows link causes to effects; two-headed arrows indicate correlations. Genes and environments are both causal inputs into an interactive developmental system (represented by the network of arrows in the center of the figure), but because people select and shape their own environments (as represented by lighter one-headed arrows from personality to environments), correlations across the developmental system (dotted two-headed arrows) are easier to detect for genes than for environments.
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However, the quasi-experimental gift of genetically identical and nonidentical twins offers a remark- able, if deceptively simple, method to span this daunting interactive complexity. Thanks to the fact that identical twins are on average ex- actly twice as similar genetically as nonidentical twins, one can use straightforward statistical procedures to estimate the proportion of variability in complex outcomes that is associated with causally dis- tant genes, all the while maintain- ing a state of near-perfect ignorance about the actual causal processes that connect genes to be- havior.
This methodological short- cut is not available to rivals of be- h a v i o r g e n e t i c s w h o s e e k t o measure the effects of families on behavior. How similar was my rearing environment to that of my siblings? And how similar was it to the environment of my adopted sibling, if I have one, or to the en- vironment of my biological sibling who was raised by someone else?
The apparent victory of nature over nurture suggested by the first two laws is thus seen to be more methodological than substantive. In a world in which there were oc- casional occurrences of “identical environmental twins,” whose ex- periences were exactly the same, moment by moment, and another variety who shared exactly (but randomly) 50% of their experi- ences, environmentalists could re- produce the precision of their ri- v a l s , a n d l i k e t h e b e h a v i o r geneticists could measure with great precision the total contribu- tion of the environment while knowing almost nothing about the developmental processes that un- derlie it.
The old-fashioned nature-nur- ture debate was about whether or not genes influence complex be- havioral outcomes, and that ques- tion has been decisively answered in the affirmative. The new ques- tion is how we can proceed from
partitioning sources of variance to specifying concrete developmental processes (Turkheimer, 1998), and although critics like Gottlieb are correct that heritability per se has few implications for a scientific un- derstanding of development, they have failed to emphasize two cru- cial points. First, heritability does have one certain consequence: It is no longer possible to interpret cor- relations among biologically re- lated family members as prima fa- cie evidence of sociocultural causal mechanisms.
If the children of de- pressed mothers grow up to be de- pressed themselves, it does not necessarily demonstrate that being raised by a depressed mother is it- self depressing. The children might have grown up equally depressed if they had been adopted and raised by different mothers, under the influence of their biological mother’s genes.
For every behavior geneticist who continues to report moderate heritabilities as though they were news, there is an envi- ronmentalist who reports causally ambiguous correlations between genetically related parents and children. Second, the problem the critics have uncovered extends well beyond behavior genetics: It is a rare environmentalist who has never used statistical methods to predict behavioral outcomes from earlier events, in the hope that the specific developmental mecha- nisms can be filled in later.
The dis- connect between the analysis of variance and the analysis of causes, to use Lewontin’s (1974) phrase, is not a proprietary flaw in behavior genetic methodology; in fact, it is the bedrock methodological prob- lem of contemporary social science.
NONSHARED ENVIRONMENT AND THE
Even after the effects of genes and the shared effects of families
have been accounted for, around 50% of the differences among sib- lings is left unexplained. In recent years, scientists interested in the genetics of behavior have come to call this unexplained portion the “nonshared environment.” Al- though according to the second law shared environment accounts for a small proportion of the variability in behavioral outcomes, ac- cording to the third law, nonshared environment usually accounts for a substantial portion.
So perhaps the appropriate conclusion is not so much that the family environment does not matter for development, but rather that the part of the fam- ily environment that is shared by siblings does not matter. What does matter is the individual envi- ronments of children, their peers, and the aspects of their parenting that they do not share. Plomin and Daniels (1987) reviewed evidence of the predominance of nonshared environmental variance and posed a seminal question: Why are chil- dren in the same family so differ- ent?
They proposed that siblings are different because nonshared environmental events are more potent causes of developmental outcomes than the shared environ- mental variables, like socioeco- nomic status, that have formed the traditional basis of sociocultural developmental psychology.
Plomin and Daniels’s explana- tion involves a subtle conceptual shift, best described in terms of a distinction between the objective and effective environment (Gold- smith, 1993; Turkheimer & Wal- dron, 2000). What qualifies an en- vironmental event as nonshared?
There are two possibilities. The first is objective: An event is non- shared if it is experienced by only one sibling in a family, regardless of the consequences it produces. The other possibility is effective: An environmental event is non- shared if it makes siblings different
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rather than similar, regardless of whether it was experienced by one or both of them. Plomin and Daniels’s proposal, then, is that the nonshared environment as an ef- fectively defined variance compo- nent can be explained by objec- tively nonshared environmental events. The question, “Why are children in the same family so dif- ferent?” is answered, “Because measurable differences in their en- vironments make them that way.”
This proposal has been enor- mously influential, spawning an entire area of empirical inquiry into the consequences of measured en- vironmental differences among siblings. Ironically, that same lit- erature has quite decisively dem- onstrated that the conjecture is false.
A review of 43 studies that measured differences in the envi- ronments of siblings and related them to differences in the siblings’ developmental outcomes (Turk- heimer & Waldron, 2000) has shown that although upwards of 50% of the variance in behavioral outcomes is accounted for by the effectively defined variance com- ponent called nonshared environ- ment, the median percentage ac- counted for by objectively defined nonshared events is less than 2%. What could be going on?
Plomin and Daniels (1987) al- most identified the answer to this question, but dismissed it as too pessimistic:
One gloomy prospect is that the salient environment might be unsystematic, idiosyncratic, or serendipitous events such as accidents, illnesses, or other traumas . . . . Such capricious events, however, are likely to prove a dead end for research. More interesting heuristi- cally are possible systematic sources of differences between families. (p. 8)
The gloomy prospect is true. Non- shared environmental variability predominates not because of the systematic effects of environmental events that are not shared among siblings, but rather because of the unsystematic effects of all environ- mental events, compounded by the equally unsystematic processes that expose us to environmental events in the first place (Turk- heimer & Gottesman, 1996).
A model of nonshared variabil- ity based on the gloomy prospect is radically different from the Plomin model based on systematic conse- quences of environmental differ- ences among siblings. Most impor- tant, the two models suggest very different prospects for a genetically informed developmental psychol- ogy.
Again and again, Plomin and his colleagues have emphasized that the importance of nonshared environment implies that it is time to abandon shared environmental variables as possible explanations of developmental outcomes. And although modern environmental- ists might not miss coarse mea- sures like socioeconomic status, it is quite another thing to give up on the causal efficaciousness of nor- mal families, as Scarr (1992), Rowe (1994), and Harris (1998) have urged.
If, however, nonshared en- vironmental variability in outcome is the result of the unsystematic consequences of both shared and nonshared environmental events, the field faces formidable method- ological problems—Plomin and Daniels’s gloomy prospect—but need not conclude that aspects of families children share with sib- lings are of no causal importance.
CONCLUSION: ANTICIPATING THE GENOME PROJECT
It is now possible for behavior genetics to move beyond statistical analyses of differences between identical and nonidentical twins and identify individual genes that are related to behavioral outcomes.
What should we expect from this endeavor? Behavior geneticists an- ticipate vindication: At long last, statistical variance components will be rooted in the actual causal consequences of actual genes. Crit- ics of behavior genetics expect the opposite, pointing to the repeated failures to replicate associations be- tween genes and behavior as evi- dence of the shaky theoretical un- derpinnings of which they have so long complained.
There is an interesting parallel between the search for individual genes that influence behavior and the failed attempt to specify the nonshared environment in terms of measured environmental variables. In each case, investigators began with statistically reliable but caus- ally vague sources of variance, and set out to discover the actual causal processes that produced them.
The quest for the nonshared environ- ment, as we have seen, got stuck in the gloomy prospect. Although in- dividual environmental events in- fluence outcomes in the most gen- eral sense, they do not do so in a systematic way. One can detect their effects only by accumulating them statistically, using twins or adoptees.
If the underlying causal struc- ture of human development is highly complex, as illustrated in Figure 1, the relatively simple sta- tistical procedures employed by developmental psychologists, ge- neticists, and environmentalists alike are being badly misapplied. But misapplied statistical proce- dures still produce what appear to be results.
Small relations would still be found between predictors and outcomes, but the underlying complex causal processes would cause the apparent results to be small, and to change unpredictably from one experiment to the next. So individual investigators would ob- tain “results,” which would then fail to replicate and accumulate into a coherent theory because the
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simple statistical model did not fit the complex developmental pro- cess to which it was being applied. Much social science conducted in the shadow of the gloomy prospect has exactly this flavor (e.g., Meehl, 1978).
The gloomy prospect looms larger for the genome project than is generally acknowledged. The question is not whether there are correlations to be found between individual genes and complex be- havior—of course there are—but instead whether there are domains of genetic causation in which the gloomy prospect does not prevail, allowing the little bits of correla- tional evidence to cohere into rep- licable and cumulative genetic models of development.
My own prediction is that such domains will prove rare indeed, and that the likelihood of discovering them will be inversely related to the com- plexity of the behavior under study.
Finally, it must be remembered that the gloomy prospect is gloomy only from the point of view of the working social scientist. Although frustrated developmental psy- chologists may be tempted to favor methodologically tractable heuris-
In the long run, the gloomy prospect al- ways wins, and no one would want to live in a world where it did not. Psychology is at least one good paradigm shift away from an em- pirical answer to the gloomy pros- pect, but the philosophical re- sponse is becoming clear: The additive effect of genes may con- stitute what is predictable about human development, but what is predictable about human develop- ment is also what is least interest- ing about it. The gloomy prospect isn’t.
References Goldsmith, H. (1993). Nature-nurture issues in the
behavioral genetic context: Overcoming barri- ers to communication. In R. Plomin & G. Mc- Clearn (Eds.), Nature, nurture and psychology (pp. 325–339). Washington, DC: American Psychological Association.
Gottlieb, G. (1991). Experiential canalization of be- havioral development: Theory. Developmental Psychology, 27, 4–13.
Gottlieb, G. (1992). Individual development and evo- lution. New York: Oxford University Press.
Gottlieb, G. (1995). Some conceptual deficiencies in “developmental” behavior genetics. Human Development, 38, 131–141.
Harris, J.R. (1998). The nurture assumption: Why children turn out the way they do. New York: Free Press.
Lewontin, R.C. (1974). The analysis of variance and the analysis of causes. American Journal of Human Genetics, 26, 400–411.
Meehl, P.E. (1978). Theoretical risks and tabular asterisks: Sir Karl, Sir Ronald, and the slow progress of soft psychology. Journal of Consult- ing and Clinical Psychology, 46, 806–834.
Plomin, R., & Daniels, D. (1987). Why are children in the same family so different from one an- other? Behavioral and Brain Sciences, 10, 1–60.
Rowe, D.C. (1994). The limits of family influence: Genes, experience, and behavior. New York: Guil- ford Press.
Scarr, S. (1992). Developmental theories for the 1990s: Development and individual differ- ences. Child Development, 63, 1–19.
Turkheimer, E. (1998). Heritability and biological explanation. Psychological Review, 105, 782–791.
Turkheimer, E., Goldsmith, H.H., & Gottesman, I.I. (1995). Commentary. Human Development, 38, 142–153.
Turkheimer, E., & Gottesman, I.I. (1991). Is H2 = 0 a null hypothesis anymore? Behavioral and Brain Sciences, 14, 410–411.
Turkheimer, E., & Gottesman, I.I. (1996). Simulat- ing the dynamics of genes and environment in development. Development and Psychopathol- ogy, 8, 667–677.
Turkheimer, E., & Waldron, M.C. (2000). Non- shared environment: A theoretical, method- ological, and quantitative review. Psychological Bulletin, 126, 78–108.
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