Twin studies are one of a family of designs in behavior genetics which aid the study of individual differences by highlighting the role of environmental and genetic causes on behavior. Twins are invaluable for studying these important questions because they disentangle the sharing of genes and environments. If we observe that children in a family are more similar than might be expected by chance, this may reflect shared environmental influences common to members of family —class, parenting styles, education etc.— but they will also reflect shared genes, inherited from parents. The twin design compares the similarity of identical twins who share 100% of their genes, to that of dizygotic or fraternal twins, who share only 50% of their genes. By studying many hundreds of families of twins, researchers can then understand more about the role of genetic effects, and the effects of shared and unique environment effects.

Modern twin studies have shown that almost all traits are in part influenced by genetic differences, with some characteristics showing a strong influence (e.g., height), others an intermediate level (i.e. IQ) and some more complex heritabilities, with evidence for different genes affecting different elements of the trait - for instance Autism.

History

Francis Galton laid the foundations of behavior genetics as a branch of science.

While twins have been of interest to scholars since early civilization, such as the early physician Hippocrates (5th c. BCE), who attributed similar diseases in twins to shared material circumstances, and the stoic philosopher Posidonius (1rst c. BCE), who attributed such similarities to shared astrological sex circumstances, the modern history of the twin study derives from Sir Francis Galton's pioneering use of twins to study the role of genes and environment on human development and behavior.

Methods

The power of twin designs arises from the fact that twins may be either monozygotic (MZ: developing from a single fertilized egg and therefore sharing all of their genes) – or dizygotic (DZ: developing from two fertilized eggs and therefore sharing on average 50% of their genes, the same level of genetic similarity as found in non-twin siblings). These known differences in genetic similarity, together with a testable assumption of equal environments for MZ and DZ twins (Bouchard & Propping, 1993) creates the basis for the twin design for exploring the effects of genetic and environmental variance on a phenotype (Neale & Cardon, 1992).

The basic logic of the twin study can be understood with very little mathematics beyond an understanding of correlation and the concept of variance.

Like all behavior genetic research, the classic twin study begins from assessing the variance of a behavior (called a phenotype by geneticists) in a large group, and attempts to estimate how much of this is due to genetic effects (heritability), how much appears to be due to shared environmental effects, and how much is due to unique environmental effects - events occurring to one twin but not another.

Typically these three components are called A (additive genetics) C (common environment) and E (unique environment). the so-called ACE Model. It is also possible to examine non-additive genetics effects (often denoted D for dominance (see below for more complex twin designs).

Given the ACE model, researchers can determine what proportion of variance in a trait is heritable, versus the proportions which are due to shared environment or unshared environment. While nearly all research is carried out using SEM programs such as the freeware Mx, the essential logic of the twin design is as follows:

MZ twins raised in a family share both 100% of their genes, and all of the shared environment. All differences between them in this framework are unique. The correlation we observe between MZ twins provides an estimate of A+C. DZ twins have a common shared environment, and share 50% of their genes: so the correlation between DZ twins is a direct estimate of 1/2A + C.

r_MZ = A+C

r_DZ = .5*A+C

These two equations allow us to derive A C and E:

A = 2*(r_mz- r_dz)

C = r_mz-A

E= 1-r_mz

Where r_mz and r_dz are simply the correlations of the trait in MZ and DZ twins respectively. Twice difference between MZ and DZ twins gives us A: the additive genetic effect. C is simply the MZ correlation - our estimate of A, and E is estimated directly by how much the MZ twin correlation deviates from 1. (Jinks & Fulker, 1970; Plomin, DeFries , McClearn, & McGuffin, 2001).

Modern Modeling

Beginning in the 1970s, research transitioned to explicitly modeling the values of A, C, and E within a maximum likelihood framework (Martin & Eaves, 1977). While computationally much more complex, benefits of this approach are manifold, and modeling tools such as Mx (Neale, Boker, Xie, & Maes, 2002) have made the new techniques relatively accessible.

Assumptions

Equal environments. It can be seen from the modelling above, that the main assumption of the twin study is that of equal environments. At an intuitive level, this seems reasonable - why would parents note that two children shared their hair and eye color, and then contrive to make their IQs identical? Indeed, how could they? This assumption, however, has been directly tested. An interesting case occurs where parents believe their twins to be non-identical when in fact they are genetically MZ. Studies of a range of psychological traits indicate that these children remain as concordant as MZs raised by parents who treated them as identical (Kendler, Neale, Kessler, Heath, & Eaves, 1993).

Measured similarity: A direct test of assumptions in twin designs

A particularly powerful technique for testing the twin method has recently been reported by Visscher et al. Instead of using twins, this group took advantage of the fact that while siblings on average share 50% of their genes, the actual gene-sharing for individual sibling pairs varies around this value, essentially creating a continuum of genetic similarity or "twinness" within families. Estimates of heritability based on direct estimates of gene sharing confirm those from the twin method, providing support for the assumptions of the method in the domains of cognition, personality, and psychopathology.

Extended twin designs and more complex genetic models

The basic or classical twin-design contains only MZ and DZ twins raised in their biological family. This represents only a sub-set of the possible genetic and environmental relationships. It is fair to say, therefore, that the heritability estimates from twin designs represent a first step in understanding the genetics of behavior. The variance partitioning of the twin study into additive genetic, shared, and unshared environment is a first approximation to a complete analysis taking into account gene-environment covariance and interaction, as well as other non-additive effects on behavior. The revolution in molecular genetics has provided more effective tools for describing the genome, and many researchers are pursuing molecular genetics in order to directly assess the influence of alleles and environments on traits.

An initial limitation of the twin design is that is does not afford an opportunity to consider both Shared Environment and Non-additive genetic effects simultaneously. This limit can be addressed by including additional siblings to the design.

A second limitation is that GE correlation is not detectable as a distinct effect. Addressing this limit requires incorporating adoption models, or children-of-twins designs, to assess family influences uncorrelated with shared genetic effects.

Criticism

The Twin Method has been subject to criticism from Statistical Genetics, Statistics and Psychology, with some^{[weasel words]} arguing that conclusions reached via this method are ambiguous or meaningless. Core elements of these criticisms and their rejoinders are listed below:

Criticisms of Statistical Methods

It has been argued that that the Statistical underpinnings of twin research are invalid. Such statistical critiques argue that heritability estimates used for most twin studies rest on restrictive assumptions which are usually not tested, and if they are, are often found to be violated by the data.

For example, Peter Schonemann has criticized methods for estimating heritability developed in the 1970s. He has also argued that the heritability estimate from a twin study may reflect factors other than shared genes. Using the statistical models published in Loehlin and Nichols (1976)^[1], the narrow heritability’s of HR of responses to the question “did you have your back rubbed” has been shown to work out to .92 heritable for males and .21 heritable for females, and the question “Did you wear sunglasses after dark?” is 130% heritable for males and 103% for females ^{[2] [3]}

Responses to Statistical Critiques

In the days before the computer, statisticians were forced to use methods which were computationally tractable, at the cost of known limitations. Since the 1980s these approximate statistical methods have been discarded: Modern twin methods based on Structural Equation Modeling are not subject to the limitations and heritability estimates such as those noted above are impossible. Critically, the newer methods allow for explicit testing of the role of different pathways and incorporation and testing of complex effects.

Sampling: Twins as representative members of the population

The results of twin studies cannot be automatically generalized beyond the population in which they have been derived. It is therefore important to understand the particular sample studied, and the nature of twins themselves.

Twins are not a random sample of the population, and they differ in their developmental environment. In this sense they are not representative ^[4]

For example: Dizygotic (DZ) twin births are affected by many factors. Some women frequently produce more than one egg at each menstrual period and, therefore, are more likely to have twins. This tendency may run in the family either in the mother's or father's side of the family, and often runs through both. Women over the age of 35 are more likely to produce two eggs. Women who have three or more children are also likely to have dizygotic twins. Artificial induction of ovulation and in vitro fertilization-embryo replacement can also give rise to DZ and MZ twins ^{[5] [6] [7][8] [9] [10]}.

Response to representativeness of twins

Twins differ very little from non-twin siblings. Measured studies on the personality and intelligence of twins suggest that they have scores on these traits very similar to those of non-twins (for instance Deary et al. 2006).

Observational nature of twin studies

For very obvious reasons, studies of twins are with almost no exceptions observational. This contrasts with, for instance, studies in plants or in animal breeding where the effects of experimentally randomized genotypes and environment combinations are measured. In human studies, we observe rather than control the exposure of individuals to different environments. ^{[11] [12] [13] [14]}

Response to the observational nature of twin studies

The observational study and its inherent confounding of causes is common in psychology. Twin studies are in part motivated by an attempt to take advantage of the random assortment of genes between members of a family to help understand these correlations. Thus, while the twin study tells us only how genes and families affect behavior within the observed range of environments, and with the caveat that often genes and environments will covary, this is argued to be a considerable advance over the alternative, which is no knowledge of the different roles of genes and environment whatsoever.

Advanced Methodology

Interactions

The effects of genes depend on the environment they are in. Possible complex genetic effects include G*E interactions, in which the effects of a gene allele differ across different environments. Simple examples would include situations where a gene multiples the effect of an environment (in this case the slope of response to an environment would differ between genotypes). A second effect is "GE correlation", in which certain allelles occur more frequently than others in certain environments. If a gene causes a person to enjoy reading, then children with this allele are likely to be raised in households with books in them (due to GE correlation: one or both of their parents has the allele and therefore both accumulates a book collection and passes on the book-reading allele). Such effects can be assessed by measuring the purported environmental correlate (in this case books in the home) directly.

Often the role of environment seems maximal very early in life, and decreases rapidly after compulsory education begins. This is observed for instance in reading (Byrne etal 2006) as well as intelligence (Deary et al, 2006). This is an example of a G*Age effect and allows an examination of both GE correlations due to parental environments (these are broken up with time), and of G*E correlations caused by individuals actively seeking certain environments (Plomin et al., 1987).

Continuous variable or Correlational studies

While concordance studies compare traits which are either present or absent in each twin, correlational studies compare the agreement in continuously varying traits across twins.

Fig 2. Heritability for nine psychological traits as estimated from twin studies. All sources are twins raised together (sample size shown inside bars). As outlined above, identical twins (MZ twins) are twice as genetically similar as fraternal twins (DZ twins) and so heritability (h²) is approximately twice the difference in correlation between MZ and DZ twins. Unique environmental variance (e²) is reflected by the degree to which identical twins raised together are dissimilar, and is approximated by 1-MZ correlation. The effect of shared environment (c²) contributes to similarity in all cases and is approximated by the DZ correlation minus the difference between MZ and DZ correlations.

Terminology

Pairwise concordance

Fig 1. Twin concordances for seven psychological traits (sample size shown inside bars).

For a group of twins, pairwise concordance is defined as C/(C+D), where C is the number of concordant pairs and D is the number of discordant pairs.

For example, a group of 10 twins have been pre-selected to have one affected member (of the pair). During the course of the study four other previously non-affected members become affected, giving a pairwise concordance of 4/(4+6) or 4/10 or 40%.

Probandwise concordance

For a group of twins in which at least one member of each pair is affected, probandwise concordance is a measure of the proportion of twins who have the illness who have an affected twin and can be calculated with the formula of 2C/(2C+D), in which C is the number of concordant pairs and D is the number of discordant pairs.

For example, consider a group of 10 twins that have been pre-selected to have one affected member. During the course of the study, four other previously non-affected members become affected, giving a probandwise concordance of 8/(8+6) or 8/14 or 57%.

Further reading

• Textbook, software, and example scripts for twin research
• Jang, K.L., McCrae, R.R., Angleitner, A. Riemann, R. & Livesley, W.J. (1998). Heritability of facet-level traits in a cross-cultural twin sample: support for a hierarchical model of personality. Journal of Personality and Social Psychology 74:1556-1565.
• Plomin, DeFries, McClearn & McGuffin (2000). Behavioral Genetics: A Primer 4th edition. W.H.Freeman & Co Ltd.
• Nancy L. Segal (2005) Indivisible by Two: Lives of Extraordinary Twins. New York, Harvard University Press.

Critical Accounts

• Peter Schonemann (1997). Models and muddles of heritability. Genetica, 99, 97-108: [1]
• Peter Schonemann and Roberta D. Schonemann (1994). Environmental versus genetic models for Osborne’s personality data on identical and fraternal twins. CPC, 1994, 13 (2), 141-167 [2]
• Kamin, L. J. (1974). The Science and Politics of I.Q. Potomac, MD: Lawrence Erlbaum Associates.
• Kempthorne O. (1997). Heritability: uses and abuses. Genetica, Volume 99, Numbers 2-3, 1997 , pp. 109-112(4)
• Joseph, J. (2003). The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope. PCCS Books.

This book has been critically reviewed for the American Psychological Association. Hanson, D. R. (2005). 'The Gene Illusion Confusion: A review of The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope by Jay Joseph' [Electronic Version]. PsycCritiques, 50, e14.

• Christiane Capron, Adrian R. Vetta, Michel Duyme and Atam Vetta (1999). Misconceptions of biometrical IQists. Cahiers de Psychologie Cognitive/Current Psychology of Cognition 1999, 18 (2), 115-160
• Horwitz AV, Videon TM, Schmitz MF, Davis D. Rethinking twins and environments: possible social sources for assumed genetic influences in twin research. J Health Soc Behav. 2003 Jun;44(2):111-129.

And in reply to this article see:

• Freese J and Powell B Tilting at Twindmills: rethinking sociological responses to behavioral genetics. J Health Soc Behav. 2003 Jun;44(2):130-135.

See also

• Behavioral genetics
• Gene-environment interaction
• Heritability
• Human nature
• Identical Strangers: A Memoir of Twins Separated and Reunited
• Nature versus nurture

External links

Several academic bodies exist to support behavior genetic research, including the Behavior Genetics Association [3], the International Society for Twin Studies, and the International Behavioural and Neural Genetics Society [4]. Behavior genetic work features prominently in several more general societies, for instance the International Society of Psychiatric Genetics. [5]

The following Twin Studies are ongoing studies that are recruiting subjects:

• Maudsley Bipolar Twin Study, London, UK (Home page)

• The Twin Research Unit (King's College London) UK

• University of Pennsylvania Sleep Research Study for Twins

• List of Current Twin Studies

References

The nature versus nurture debates concern the relative importance of an individual's innate qualities ("nature", i.e. nativism, or philosophical empiricism, innatism) versus personal experiences ("nurture") in determining or causing individual differences in physical and behavioral traits. The view that humans acquire all or almost all their behavioral traits from "nurture" is known as tabula rasa ("blank slate"). This question was once considered to be an appropriate division of developmental influences, but since both types of factors are known to play such interacting roles in development, many modern psychologists consider the question naive - representing an outdated state of knowledge^[1][2][3]. The famous psychologist Donald Hebb is said to have once answered a journalist's question of "which, nature or nurture, contributes more to personality?" by asking in response, "which contributes more to the area of a rectangle, its length or its width?"^[4][5][6][7]. For a discussion of nature versus nurture in language and other human universals, see also psychological nativism.

Scientific approach

In order to disentangle the effects of genes and environment, behavioral geneticists perform adoption and twin studies. Behavioral geneticists do not generally use the term "nurture" in order to explain that portion of the variance for a given trait (such as IQ or the Big Five personality traits) that can be attributed to environmental effects. Instead, two different types of environmental effects are distinguished: shared family factors (i.e., those shared by siblings, making them more similar) and nonshared factors (i.e., those that uniquely affect individuals, making siblings different). In order to express the portion of the variance that is due to the "nature" component, behavioral geneticists generally refer to the heritability of a trait.

With regard to the Big Five personality traits as well as adult IQ in the general U.S. population, the portion of the overall variance that can be attributed to shared family effects is often negligible. ^[8] On the other hand, most traits are thought to be at least partially heritable. In this context, the "nature" component of the variance is generally thought to be more important than that ascribed to the influence of family upbringing.

In her Pulitzer Prize-nominated book The Nurture Assumption, author Judith Harris argues that "nurture," as traditionally defined in terms of family upbringing does not effectively explain the variance for most traits (such as adult IQ and the Big Five personality traits) in the general population of the United States. On the contrary, Harris suggests that either peer groups or random environmental factors (i.e., those that are independent of family upbringing) are more important than family environmental effects ^{[9] [10]}

Although "nurture" has historically been referred to as the care given to children by the parents, with the mother playing a role of particular importance, this term is now regarded by some as any environmental (not genetic) factor in the contemporary nature versus nurture debate. Thus the definition of "nurture" has been expanded in order to include the influences on development arising from prenatal, parental, extended family and peer experiences, extending to influences such as media, marketing and socio-economic status. Indeed, a substantial source of environmental input to human nature may arise from stochastic variations in prenatal development.

Heritability estimates

This chart illustrates three patterns one might see when studying the influence of genes and environment on traits in individuals. Trait A shows a high sibling correlation, but little heritability (i.e. high shared environmental variance c²; low heritability h²). Trait B shows a high heritability since correlation of trait rises sharply with degree of genetic similarity. Trait C shows low heritability, but also low correlations generally; this means Trait C has a high nonshared environmental variance e². In other words, the degree to which individuals display Trait C has little to do with either genes or broadly predictable environmental factors—roughly, the outcome approaches random for an individual. Notice also that even identical twins raised in a common family rarely show 100% trait correlation.

While there are many examples of single-gene-locus traits, current thinking in biology discredits the notion that genes alone can determine most complex traits. At the molecular level, DNA interacts with signals from other genes and from the environment. At the level of individuals, particular genes influence the development of a trait in the context of a particular environment. Thus, measurements of the degree to which a trait is influenced by genes versus environment will depend on the particular environment and genes examined. In many cases, it has been found that genes may have a substantial contribution, including psychological traits such as intelligence and personality^[11]. Yet, these traits may be largely influenced by environment in other circumstances, such as environmental deprivation.

A researcher seeking to quantify the influence of genes or environment on a trait needs to be able to separate the effects of one factor away from that of another. This kind of research often begins with attempts to calculate the heritability of a trait. Heritability quantifies the extent to which variation among individuals in a trait is due to variation in the genes those individuals carry. In animals where breeding and environments can be controlled experimentally, heritability can be determined relatively easily. Such experiments would be unethical for human research. This problem can be overcome by finding existing populations of humans that reflect the experimental setting the researcher wishes to create.

One way to determine the contribution of genes and environment to a trait is to study twins. In one kind of study, identical twins reared apart are compared to randomly selected pairs of people. The twins share identical genes, but different family environments. In another kind of twin study, identical twins reared together (who share family environment and genes) are compared to fraternal twins reared together (who also share family environment but only share half their genes). Another condition that permits the disassociation of genes and environment is adoption. In one kind of adoption study, biological siblings reared together (who share the same family environment and half their genes) are compared to adoptive siblings (who share their family environment but none of their genes).

Some have rightly pointed out that environmental inputs affect the expression of genes. This is one explanation of how environment can influence the extent to which a genetic disposition will actually manifest. The interactions of genes with environment, called gene-environment interaction, are another component of the nature-nurture debate. A classic example of gene-environment interaction is the ability of a diet low in the amino acid phenylalanine to partially suppress the genetic disease phenylketonuria. Yet another complication to the nature-nurture debate is the existence of gene-environment correlations. These correlations indicate that individuals with certain genotypes are more likely to find themselves in certain environments. Thus, it appears that genes can shape (the selection or creation of) environments. Even using experiments like those described above, it can be very difficult to determine convincingly the relative contribution of genes and environment.

Interaction of genes and environment

In only a very few cases is it fair to say that a trait is due almost entirely to nature, or almost entirely to nurture. In the case of most diseases now strictly identified as genetic, such as Huntington's disease, there is a better than 99.9% correlation between having the identified gene and the disease and a similar correlation for not having either. On the other hand, such traits as one's native language are entirely environmentally determined: linguists have found that any child (if capable of learning a language at all) can learn any human language with equal facility. With virtually all psychological traits however, there is an intermediate mix of nature and nurture, and opinions about the relative importance of each will often vary widely.

Examples of environmental, interactional, and genetic traits are:

The "two buckets" view of heritability.

More realistic "homogenous mudpie" view of heritability.

Steven Pinker (2004) likewise described several examples:

concrete behavioral traits that patently depend on content provided by the home or culture—which language one speaks, which religion one practices, which political party one supports—are not heritable at all. But traits that reflect the underlying talents and temperaments—how proficient with language a person is, how religious, how liberal or conservative—are partially heritable.

When traits are determined by a complex interaction of genotype and environment it is possible to measure the heritability of a trait within a population. However, many non-scientists who encounter a report of a trait having a certain percentage heritability, imagine non-interactional, additive contributions of genes and environment to the trait. As an analogy, some laypeople may think of the degree of a trait being made up of two "buckets", genes and environment, each able to hold a certain capacity of the trait. But even for intermediate heritabilities, a trait is always shaped by both genetic dispositions and the environments in which people develop, merely with greater and lesser plasticities associated with these heritability measures.

Heritibility measures always refer to the degree of variation between individuals in a population. These statistics cannot be applied at the level of the individual. It is incorrect to say that since the heritiability index of personality is about .6, you got 60% of your personality from you parents, and 40% from the environment. To help to understand this, imagine that all humans were genetic clones. The heritiability index for all traits would be zero (all variability between clonal individuals must be due to environmental factors). And, contrary to erroneous interpretations of the heritibility index, as societies become more egalitarian (everyone has more similar experiences), the heritability index goes up (as environments become more similar, variability between individuals is due more to genetic factors).

A highly genetically loaded trait (such as eye color) still assumes environmental input within normal limits (a certain range of temperature, oxygen in the atmosphere, etc.). A more useful distinction than "nature vs. nurture" is "obligate vs. facultative" -- under typical environmental ranges, what traits are more "obligate" (e.g., the nose -- everyone has a nose) or more "facultative" (sensitive to environmental variations, such as specific language learned during infancy). Another useful distinction is between traits that are likely to be adaptations (such as the nose) vs. those that are byproducts of adaptations (such the white color of bones), or are due to random variation (non-adaptive variation in, say, nose shape or size).

Nature versus nurture in the IQ debate

Evidence suggests that family environmental factors may have an effect upon childhood IQ, accounting for up to a quarter of the variance. On the other hand, by late adolescence this correlation disappears, such that adoptive siblings are no more similar in IQ than strangers.^[12] Moreover, adoption studies indicate that, by adulthood, adoptive siblings are no more similar in IQ than strangers (IQ correlation near zero), while full siblings show an IQ correlation of 0.6. Twin studies reinforce this pattern: monozygotic (identical) twins raised separately are highly similar in IQ (0.86), more so than dizygotic (fraternal) twins raised together (0.6) and much more than adoptive siblings (~0.0). ^[13] Consequently, in the context of the "nature versus nurture" debate, the "nature" component appears to be much more important than the "nurture" component in explaining IQ variance in the general adult population of the United States.

Nature versus nurture in personality traits

Personality is a frequently cited example of a heritable trait that has been studied in twins and adoptions. Identical twins reared apart are far more similar in personality than randomly selected pairs of people. Likewise, identical twins are more similar than fraternal twins. Also, biological siblings are more similar in personality than adoptive siblings. Each observation suggests that personality is heritable to a certain extent. However, these same study designs allow for the examination of environment as well as genes. Adoption studies also directly measure the strength of shared family effects. Adopted siblings share only family environment. Unexpectedly, some adoption studies indicate that by adulthood the personalities of adopted siblings are no more similar than random pairs of strangers. This would mean that shared family effects on personality are zero by adulthood. As is the case with personality, non-shared environmental effects are often found to out-weigh shared environmental effects. That is, environmental effects that are typically thought to be life-shaping (such as family life) may have less of an impact than non-shared effects, which are harder to identify. One possible source of non-shared effects is the environment of pre-natal development. Random variations in the genetic program of development may be a substantial source of non-shared environment. These results suggest that "nurture" may not be the predominant factor in "environment".

Advanced techniques

The power of quantitative studies of heritable traits has been expanded by the development of new techniques. Developmental genetic analysis examines the effects of genes over the course of a human lifespan. For example, early studies of intelligence, which mostly examined young children, found heritability measures of 40 to 50 percent. Subsequent developmental genetic analyses have found that genetic contribution to intelligence increases over a lifespan,^[14][15][16] reaching a heritability of 80 percent in adulthood.

Another advanced technique, multivariate genetic analysis, examines the genetic contribution to several traits that vary together. For example, multivariate genetic analysis has demonstrated that the genetic determinants of all specific cognitive abilities (e.g., memory, spatial reasoning, processing speed) overlap greatly, such that the genes associated with any specific cognitive ability will affect all others. Similarly, multivariate genetic analysis has found that genes that affect scholastic achievement completely overlap with the genes that affect cognitive ability.

Extremes analysis, examines the link between normal and pathological traits. For example, it is hypothesized that a given behavioral disorder may represent an extreme of a continuous distribution of a normal behavior and hence an extreme of a continuous distribution of genetic and environmental variation. Depression, phobias, and reading disabilities have been examined in this context.

For highly heritable traits, it is now possible to search for individual genes that contribute to variation in that trait. For example, several research groups have identified genetic loci that contribute to schizophrenia (Harrison and Owen, 2003).

Moral difficulties: eugenics, etc.

Some observers believe that modern science tends to give too much weight to the nature side of the argument, in part because of social consciousness. Historically, much of this debate has had undertones of racist and eugenicist policies — the notion of race as a scientific truth has often been assumed as a prerequisite in various incarnations of the nature versus nurture debate. In the past, heredity was often used as "scientific" justification for various forms of discrimination and oppression along racial and class lines. Works published in the United States since the 1960s that argue for the primacy of "nature" over "nurture" in determining certain characteristics, such as The Bell Curve, have been greeted with considerable controversy and scorn.

A critique of moral arguments against the nature side of the argument could be that they cross the is-ought gap. That is, they apply values to facts. However, such appliance appears to construct reality. Belief in biologically determined stereotypes and abilities has been shown to increase the kind of behavior that is associated with such stereotypes and to impair intellectual performance through, among other things, the stereotype threat phenomenon.

Philosophical difficulties

Are the traits real?

It is sometimes a question whether the "trait" being measured is even a real thing. Much energy has been devoted to calculating the heritability of intelligence (usually the I.Q., or intelligence quotient), but there is still some disagreement as to what exactly "intelligence" is.

Biological determinism

If genes do contribute substantially to the development of personal characteristics such as intelligence and personality, then many wonder if this implies that genes determine who we are. Biological determinism is the thesis that genes determine who we are. Few if any scientists would make such a claim^[17]; however, many are accused of doing so.

Others have pointed out that the premise of the "nature versus nurture" debate seems to negate the significance of free will. More specifically, if all our traits are determined by our genes, by our environment, by chance, or by some combination of these acting together, then there seems to be little room for free will. In any case, this line of reasoning suggests that the "nature versus nurture" debate tends to exaggerate the degree to which individual human behavior can be predicted based on knowledge of genetics and the environment. It should also be pointed out that biology may determine our abilities, but free will still determines what we do with our abilities.

Is the problem real?

Many scientists feel that the very question opposing nature to nurture is a fallacy. Already in 1951, Calvin Hall in his seminal chapter^[18] remarked that the discussion opposing nature and nurture was fruitless. If an environment is changed fundamentally, then the heritability of a character changes, too. Conversely, if the genetic composition of a population changes, then heritability will also change. As an example, we may use phenylketonuria (PKU), which causes brain damage and progressive mental retardation. PKU can be treated by the elimination of phenylalanine from the diet. Hence, a character (PKU) that used to have a virtually perfect heritability is not heritable any more if modern medicine is available. Similarly, within, say, an inbred strain of mice, no genetic variation is present and every character will have a zero heritability. If the complications of gene-environment interactions and correlations (see above) are added, then it appears to many that heritability, the epitome of the nature-nurture opposition, is "a station passed".^[19]

Myths about identity

Within the debates surrounding cloning, for example, is the far-fetched contention that a Jesus or a Hitler could be "re-created" through genetic cloning. Current thinking finds this largely inaccurate, and discounts the possibility that the clone of anyone would grow up to be the same individual due to environmental variation. For example, like clones, identical twins are genetically identical, and unlike the hypothetical clones share the same family environment, yet they are not identical in personality and other traits.

See also

• Cultural anthropology
• Diathesis-stress model
• Epigenetic Theory
• Eugenics
• Gene Illusion, The (book)
• Genetic determinism
• Genetics and violence
• Harris, Judith
• Human nature
• Onion Skin Model
• Inheritance of intelligence
• Language acquisition
• Nurture Assumption, The (book)
• Race and crime
• Reimer, David
• Social determinism
• Stereotype threat
• Tabula rasa
• Twin study
• Race and genetics

References

1. ^ Ridley, M. (2003) Nature Via Nurture: Genes, Experience, and What Makes us Human. Harper Collins. ISBN 0-00-200663-4
2. ^ Carlson, N. R. et al. (2005) Psychology: the science of behaviour (3rd Canadian ed) Pearson Ed. ISBN 0-205-45769-X
3. ^ Westen, D. (2002) Psychology: Brain, Behavior & Culture. Wiley & Sons. ISBN 0-471-38754-1
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• Alarcon, M., Plomin, R., Fulker, D.W., Corley, R. & DeFries, J.C. (1998). Multivariate path analysis of specific cognitive abilities: data at 12 years of age in the Colorado Adoption Project. Behavior Genetics 28:255-264.
• Jang, K.L., McCrae, R.R., Angleitner, A. Riemann, R. & Livesley, W.J. (1998). Heritability of facet-level traits in a cross-cultural twin sample: support for a hierarchical model of personality. Journal of Personality and Social Psychology 74:1556-1565.
• Joseph, J. (2004)The Gene Illusion: Genetic Research in Psychiatry and Psychology Under the Microscope.New York: Algora. (2003 United Kingdom Edition by PCCS Books)
• Joseph, J. (2006). The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes.New York: Algora.
• Harrison PJ, Owen MJ. (2003) Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet, 361(9355), 417–9.
• Neill, J. T. (2004). Nature vs nurture in intelligence. Wilderdom.
• Pinker, S. (2004) Why nature & nurture won't go away. Dædalus.
• Plomin, R., Fulker, D. W., Corley, R. & DeFries, J. C. (1997). Nature, nurture and cognitive development from 1 to 16 years: a parent-offspring adoption study. Psychological Science 8:442-447.
• Plomin, R., DeFries, J. C., McClearn, G. E. and McGuffin, P. (2001). Behavioral Genetics (4th Ed.). New York: Freeman. ISBN 0-7167-5159-3. 
• Ridley, M. (2003). Nature Via Nurture : Genes, Experience, and What Makes Us Human. HarperCollins. ISBN 0-06-000678-1.  (republished under the title The Agile Gene : How Nature Turns on Nurture)
• Wahlsten, D. (1997). Leilani Muir versus the Philosopher King: eugenics on trial in Alberta. Genetica 99: 185-198.
• At least two Science Fiction novels have plots which bear on this debate (in very different ways from each other): Cyteen by C. J. Cherryh (1988) and The Coming of the Quantum Cats by Frederik Pohl (1986).