Genes and Politics: A New Explanation and Evaluation of Twin Study Results and Association Studies in Political Science

Political Analysis (2013) 21:350367 doi:10.
1093/pan/mps035
Genes and Politics: A New Explanation and Evaluation of Twin Study Results and Association Studies in Political Science
Doron Shultziner Department of Medical Education, Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel e-mail: doron.shultziner@mail.huji.ac.il
Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013
Edited by R. Michael Alvarez
This article offers a new explanation for the results of twin studies in political science that supposedly disclose a genetic basis for political traits. I argue that identical twins tend to be more alike than nonidentical twins because the former are more similarly affected by the same environmental conditions, but the content of those greater trait similarities is nevertheless completely malleable and determined by particular environments. The twin studies method thus can neither prove nor refute the argument for a genetic basis of political traits such as liberal and conservative preferences or voting turnout. The meaning of heritability estimates results in twin studies are discussed, as well as the definition and function of the environment in the political science twin studies. The premature attempts to associate political traits with specific genes despite countertrends in genetics are also examined. I conclude by proposing that the alternative explanation of this article may explain certain puzzles in behavioral genetics, particularly why social and political traits have higher heritability estimates than common physical and medical traits. I map the main point of disagreements with the methodology and the interpretation of its results, and delineate the main operative implications for future research.
Introduction
Recent studies have suggested there is a connection between genetic factors on the one hand, and political preferences and behavior on the other. A small but very inuential group of scholars in political science, aided by behavioral geneticists, have termed their work the new empirical biopolitics (Alford and Hibbing 2008) and genopolitics (Biuso 2008). Compared with earlier biopolitics scholarship,1 these scholars are now condent that this recent, decidedly empirical variant of biopolitics will ourish as political scientists become increasingly aware that biology does not equate with either universalism or determinism (Alford and Hibbing 2008, 185; see also Fowler and Schreiber 2008; Hatemi, Alford, et al. 2009). A major argument concerning genes and politics was rst raised in relation to the question why do people think and act politically the way they do? Alford, Funk, and Hibbing (2005) suggested that left and right political orientations and ideologies are grounded in genetic predispositions. Fowler, Baker, and Dawes (2008) made a similar argument regarding the question why do people vote? and Hatemi, Medland, and Eaves (2009) suggested that genes contribute to the gender gap in political preferences. Hatemi, Alford, et al. (2009) found that genes determine the strength of ones party identication but not the party identication itself. The primary criticisms of these
Authors note: I thank Hagar Weinberger, Elizabeth Suhay, Martin Stevens, Duc Quang Nguyen, Orly Fuhrman, and Melvin Konner, who made useful comments on the paper. My special thanks to Diane Lavett and Yechiel Barilan, who read and helped improve several drafts of this paper. I also want to thank the anonymous reviewers who contributed constructive points. 1 Application of biological theories to politics is not new (Easton 1976; Somit 1976). For insiders reflections on the biopolitics subfield and why it has not been well received, see Hines (1982), Losco (1982), Masters (1990), Somit and Peterson (1998), Alford and Hibbing (2004); see also Tooby and Cosmides (1992) and Pinker (2003).
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studies have focused on the tenability of the equal environment assumption (EEA), namely, that identical and fraternal twins are aected by equal environments (i.e., rather than by more similar environments for identical twins; see Suhay, Kalmoe, and McDermott 2007; Beckwith and Morris 2008; Charney 2008a, 2008b; Joseph 2010). Beyond this, the political science literature remained silent about this scholarship and especially about its biological arguments. The main contribution of this article is to oer an alternative explanation for the results of twin studies in political science. I argue that the genetic factor, namely, the greater genetic similarity in identical twins, can only explain why identical twins are more similar to each other in various traits compared with nonidentical twins, but this genetic factor cannot explain the specic political content or direction of these traits. In fact, the twin research design employed in political science does not and cannot actually test the hypothesis that twins and people in general are genetically predisposed to have certain political traits rather than completely opposite ones for the exact same genotype. This explanation has not yet been considered in interpreting the results of the twin studies in political science, but it may require the rethinking of some of the assumptions, interpretations, and methodologies that are used in this eld of inquiry. The analysis oered here can also contribute to current discussions and considerations on how to proceed in funding research on the possible connection between genes and politics in political science (Lupia 2011).2 It should be stressed that the alternative explanation of the twin study results I propose in this article does not posit that there are no biological dispositions which are relevant to social life and politics. Human universals and dispositions have been identied as well as their relevance to social science (e.g., Brown 1991, 1999, 2004; Pinker 2003; Shultziner 2010; Shultziner et al. 2010). My main point is that the method of comparing twins does not and cannot reveal a genetic basis of political preferences. The assertion that the comparison of traits in twin pairs could disclose a disposition for having certain political traits and not completely dierent ones is thus based on an a priori and untested assumption about what twin studies actually prove. Accordingly, this article addresses twin studies as a general method of comparing pair types of twins; it is not a critique against a particular twin study method or experiment. None of the twin study methods in political science has dealt with or tested the alternative explanation that I propose in this article. This article proceeds as follows. In Section 2, I present an alternative biological explanation to the common results of the standard twin research design that show greater correlations of trait similarities in identical twins compared with nonidentical twins. In Section 3, I discuss the problematic ways in which the concepts of heritability estimates, environment, and the genetic factor are dened and used in twin studies. In Section 4, I shortly address the attempt that has been made to associate specic genes and chromosome regions with political traits. In Section 5, I examine the wider relevance of this analysis to results and puzzles in behavioral genetics. In Section 6, I map the operative implications of this article to future research. 2 An Alternative Explanation to the Twin Studies
The twin studies method relies on comparisons of traits in monozygotic (MZ, or identical) twins and dizygotic (DZ, or fraternal) twins. Each pair of twins is assumed to be aected by an equal, yet special, environment and life history from the time of inception. It is important to stress that the comparison of twins is not a direct genetic comparison. We know nothing about the specic genetic makeup of the twins. We do know that MZ twins are born from the same fertilized egg that split and produced two embryos, and hence they are taken to be genetically identical. DZ twins are born
2
It is important to stress that this article focuses on the classic twin studies models and genetic association studies that have been published in political science. It is beyond the scope of this article to discuss other genetic approaches such as adoption studies and extended twin family studies (Hatemi et al. 2010). Those approaches have their own complications, and their results can at times contradict the results of twin studies (e.g., Feldman and Otto 1997; Keller, Medland, and Duncan 2010). For similar reasons, I do not inquire into the recent literature on personality and politics that tends to cite and be cited in twin studies (Gerber et al. 2010; Mondak et al. 2010; compare with Verhulst, Eaves, and Hatemi 2012; with Greenstein 1992; and with Winter 2003).
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from two separate eggs that were fertilized by two dierent sperms and developed in the same womb, and they share an average of 50% of their genes (identical by descent), like any other pair of siblings (the proportion of genetic makeup of full siblings was found to range between 0.374% and 0.617%; see Visscher et al. 2006). The results of greater trait resemblance in MZ compared with DZ twins have produced heritability estimates for various traits (for reviews, see Bouchard and McGue 2003; Johnson et al. 2009; Turkheimer 2000, 2004). Heritability is the proportion of phenotypic variance in the population that can be attributed to genetic dierences in that population (see the discussion on heritability in Section 3). Political scientists who used twin studies have also presented heritability estimates for left- and right-wing ideological preferences, and for political behavior such as voting turnout (Alford, Funk, and Hibbing 2005; Fowler, Baker, and Dawes 2008; Hatemi, Medland, and Eaves 2009). In this article I refer to those political preferences and behavior as political traits for short. Authors of these studies contend that the estimates indicate a genetic eect or cause in the form of genetic structures (political genotypes) that produce distinct liberal or conservative traits or political phenotypes (Alford, Funk, and Hibbing 2008). They argue that the genetic eect is not deterministic but probabilistic. Yet this does not change the basic argument that the hypothesized genetic eect is for a certain political preference or behavior. This assertion is crucial to everything that follows from twin research (see Alford, Funk, and Hibbing 2005, 155). I argue that there is indeed a biological (or genetic) explanation for the twin study results but it is not the type of genetic eect which is suggested in the literature. The central question that must be raised in this context is why MZ twin pairs tend to be more similar than DZ pairs in some of their political traits. I set aside nongenetic or environment-only explanations and focus on the biological side of the argument. The most logical explanation of the results of twin studies is that individuals with identical genomes (e.g., MZ twins) react more similarly to the same particular environmental eects compared with individuals with nonidentical genomes (e.g., DZ twins) under equivalent conditions, but the genomes do not narrowly determine the traits themselves and equally enable a wide range of possible reactions and phenotypic expressions for the exact same genome. In the context of the twin studies this would mean that MZ twins tend to be more alike on average compared with DZ twins simply because the former are identical (or at least much more genetically alike than DZ twins) and hence they are more similarly aected by the same environmental eects but the content of those greater similarities is nevertheless malleable and predominantly determined by particular environments. When the environment changes, as is often the case, the expression and content (e.g., political preference) of the trait in question could easily change as well. Put dierently, changing the environment would not necessarily aect the greater degree of trait similarity in MZ compared with DZ twins (though it could certainly do that as well) but it could have a signicant impact on the content of the trait itself. This explanation makes a distinction between the greater trait similarities in MZ twins, which is indeed due to a simple genetic factor, and the separate issue of the trait content which is shaped and altered by the environment. While this explanation is new in the twin studies context, the basic notion underpinning it has been part and parcel of biological theory for decades. As Richard Lewontin noted early in response to the debate about the heritability of social traits, A trait can have a heritability of 1.0 in a population at some time, yet could be completely altered in the future by a simple environmental change (1974, 400). To illustrate this point in relation to the twin studies, let us rst take a simple example of two pairs of plant seeds. One pair is genetically identical, and the other pair is only 50% alike. No matter in which (equal) environment we plant these two pairs of seeds, the identical pair will tend to appear more similar in the expression of their traits (phenotypes) compared with the nonidentical pair for the very simple fact that one pair is identical and the other is not. For instance, the identical seeds will tend to exhibit greater resemblance in terms of their eventual height compared with a greater variation in the height of the nonidentical seeds when each pair is inuenced by equal environments. But the height itself could vary signicantly in dierent climates or altitudes or due to other such unique conditions. The greater resemblance is indeed solely accounted for by the greater genetic similarity of the identical seeds, but the particular phenotype is not.
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Lewontins paradigmatic concept of heritability and the example above rest on an extensive body of research in branches of biology, primarily in developmental behavioral genetics, developmental evolution, and ecological developmental biology, which have established beyond any doubt that [t]he same genotype can produce astonishingly dierent phenotypes, depending on individual experience and various environmental eects (Bateson 1998, 161). Abundant examples from ecological developmental biology show that the manifested traits (the phenotypes) of various species are not predictable from their specic genetic makeup (their genotype) but crucially depend on the ecological environment in which the organism is developing (i.e., context dependency; Gilbert 2001). This dependency of varied trait expression is due to a wide array of environmental cues, which are often unpredictable, during various stages of development. At one temperature, the snapping turtle embryo becomes male; at another temperature it becomes female. Fed one diet, a female ant larva becomes a sterile worker; fed another diet, the same larva becomes an enormous fertile queen (ibid., 4). Such phenotypic expression of organisms due to environmental stimuli is also known as developmental plasticity and phenotypic plasticity (Gilbert 2001; Price, Qvarnstrom, and Irwin 2003; Sultan 2003; Bateson et al. 2004). The argument that the same genotype can be expressed in very dierent phenotypes is not a contentious issue in biology; it is more of a bedrock truth that we must consider when interpreting the twin study results. Precisely given this accepted biological premise we must ask: is it not in the genetic repertoire of the twins (and any individual for that matter) to equally and just as easily have an opposite political trait? After all, and unlike morphological traits, many political traits and preferences are clearly malleable, are not costly to change, and could easily be modied in order to meet changing circumstances (Price, Qvarnstrom, and Irwin 2003).3 An answer to this question is already suggested from within the twin study results. It should be recalled that members of MZ pairs also have dierent traits under the same environmental eects in all the twin studies. Their trait resemblance is only relative to members of DZ pairs on average; it is not absolute. Dierent traits often do result from the same shared genotype of any given pair of MZ twins. Only on statistical average do the traits of members of MZ pairs tend to be more alike relative to members of DZ pairs. Furthermore, unlike the studies in developmental biology that were noted above, twin studies do not examine the adaptive political repertoires, the possible range of political reactions, or the degree of behavioral plasticity of the individuals studied. Twin studies cannot solve these cardinal issues and are unsuitable for this purpose because this design does not test the same genotype in a variety of conditions (Gilbert 2001; Gottlieb 2003; Sultan 2003; Ross 2006). The untested assumption is that, on average, these political preferences will remain the same in dierent environments due to a genetic eect (Lewontin 1974, 409). It should be emphasized that the problem of the underlying causality assumptions of twin studies cannot be resolved by improving statistical methods or by other twin study designs. The heart of the problem is that comparing pairs of twins could not, in any statistical form, support the hypothesis that there are genetic dispositions for having certain political traits and not others.4 Arguably, this research design also cannot refute the hypothesis because even if in certain environments there were no co-twin dierences between MZ and DZ pairs on average, this would not mean that dierent genotypes could not give rise to similar traits in one set of environments and to completely disparate traits and correlations in others. At this point it should also become obvious that the real null hypothesis for the twin studies is to test whether twins (and other people) are genetically disposed to having the traits they exhibit and not completely opposite ones for the exact same genotype just as easily. Yet twin studies involve an implicit assumption that the greater trait resemblance among MZ co-twins compared with DZ co-twins is indicative that certain political traits are hereditary in the population at large. In fact, the only possible way to generalize the twin study results is by
3
On the other hand, stable political preferences, like ones party identification or ones religion, are purely environmental (see also in Hatemi, Alford, et al. 2009). 4 Compare also with the most advanced decomposition and multivariate model that does not test or solve this cardinal problem (Verhulst, Eaves, and Hatemi 2012). See also the discussion in the next section about reared-apart twins as well as the problem of calculating environmental effects into the genetic factor measurement.
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interpreting them to mean that the greater resemblance of political traits among MZ twins is due to specic political genotypes (Alford, Funk, and Hibbing 2005, 2008) or, put less crudely, due to some genetic eects (Hatemi, Alford, et al. 2009). If the greater similarity between MZ twins is simply due to a very broad and malleable range of reactions of similar genotypes to random and special environments, no conclusion can be drawn about innate dispositions for any political trait. Only if the traits in the twin studies are interpreted and framed as resulting from political genotypes that tend to shape similar political preferences in dierent environments (or that these genetic eects have a narrow norm of reaction; see Lewontin 1974, 404; Sarkar 1999; Gilbert 2001; Sultan 2003) does it make sense to argue that twins political preferences are genetically aected. And if twins specic political traits are genetically shaped, so presumably are political traits in the population at large. This, again, is not what the twin studies actually test. Thus the most obvious alternative explanation and null hypothesis are untested in these studies.
Heritability and Environment in the Twin Studies
Given the basic problems I identied above, this immediately raises the question of what the heritability estimates in twin studies really mean and whether signicant estimates are at all indicators of a genetic basis of political traits. Heritability is a much misunderstood and often misapplied concept (Visscher, Hill, and Wray 2008). In common language (though not in formal denition) it denotes a trait that is passed down from parents to ospring, such as eye or hair color, and is stable and not highly susceptible to the environment. The terms inherited or hereditary are closer to this latter meaning. But in genetics, heritability is simply a statistical estimate that is technically dened as the proportion of phenotypic variance among individuals attributable to genetic dierences in that population (e.g., Alford and Hibbing 2008, 184). As I will show in this section, this denition of heritability, while useful for some purposes (e.g., plant and livestock breeding), is least appropriate, if relevant at all, to answer the question of whether political genotypes exist. It should be stressed in advance that the limitations pertaining to heritability that I will mention are common knowledge in biology. Some of these limitations are also stated in the twin studies in political science, but not all of them (notably in the seminal paper by Alford, Funk, and Hibbing 2005). Therefore, many political scientists (and the media) often do not understand or misinterpret the results. But beside these common problems, I will observe far less obvious and more crucial points about the denition of the environment, which may help explain the twin study results. The rst thing to note about heritability is that it refers to variation of a trait across individuals in a certain population (e.g., that of MZ relative to DZ twins). The meaning of this technical denition is that heritability is a statistical estimate that can and does change both between populations, and, more importantly, in the same population under dierent environmental eects and time periods.5 Heritability estimates of this sort give only a snapshot of trait variation between MZ and DZ twins, at a specic point in time and therefore due to particular environmental eects. In Lewontins words, the result of the analysis has a historical (i.e., spatiotemporal) limitation and is not in general a statement about functional [or causal] relations (1974, 403). Such heritability estimates can be easily modied to the point of statistical insignicance by environmental eects. Thus, high heritability [estimate] says little about how dicult it is to change a trait in circumstances other than those in which it was measured (Mameli and Bateson 2006, 165). High heritability estimates do not mean that a certain trait will remain similar or stable in a dierent environment and at a later time, as opposed to what tends to be popularly assumed
5
For example, one study has shown that DZ twins in the age cohort of 1820 have greater resemblance in their political attitudes relative to MZ twins of the same cohort. After this point, the similarity correlations for MZ twins did not become stronger. Rather, the similarities among DZ co-twins dropped (Hatemi, Funk, et al. 2009). What Hatemi and his colleagues actually show is that heritability estimates can be produced not because MZ become more similar in time (as they argue) but simply due to the fact that DZ twins show less similarity in a new environment or later in life relative to MZ twins (see also Suhay, Kalmoe, and McDermott 2007; Smith et al. 2012, 24, 28; see also discussion in Section 5). Based on this technical definition, the scholars argue that their result demonstrates a genetic influence on the transmission of political attitudes in adult life or that heritability increases with age (Hatemi, Funk, et al. 2009, 1152).
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and even argued from these studies (see Alford, Funk, and Hibbing 2005, 1645, 2008; and contrast with Hatemi, Funk, et al. 2009). The second point to note about the technical denition of heritability is that it refers to variation of a trait between populations (inter-individual) at a certain point in time and environment and not to the degree of variation of that same trait within an individual (intra-individual) in all ones developmental periods and in all dierent environments (Molenaar and Campbell 2009; compare Hatemi, Funk, et al. 2009, 1143). Namely, the heritability estimates do not say anything about an individuals level of trait plasticity, so to speak. Twin study results do not say whether an individual was likely to hold a political preference for only the environment in which it was measured and less or more rigidly in later environments. Indeed, this is precisely why heritability estimates can and often do change in a population sample in a later point of time depending on various factors ranging from age, through the size of the group and methods of measurement, to socioeconomic status and ecological conditions (see also Turkheimer et al. 2003; Visscher, Hill, and Wray 2008, 261). If the environment changes, the heritability measure changes with it (Lewontin 1974; Rose 2006, 526). Yet the published literature often interprets the results to say that individuals are genetically disposed to have certain traits and not others. Alford, Funk, and Hibbing interpret their results in this way and also add that this genetic factor explains why individuals are unable to persuade one another with rational arguments (2005, 1646; Alford and Hibbing 2008, 197). Similarly misleading is to write in the abstract of a paper that genes appear to play a pivotal role in shaping the strength of an individuals party identication (Hatemi, Alford, et al. 2009, 584, emphases added). The thorny issue is how to dierentiate between the environmental causes of variation of a trait on the one hand and the genetic factor of that trait on the other. The scholars working in this eld in political science acknowledge the importance of genes and the environment, as well as the interaction between the two, in determining political traits. A typical statement is as follows: The underlying construct that is responsible for a specic trait value (phenotype) is due to some combination of genetic and environmental inuences (Hatemi, Alford, et al. 2009, 585). Yet terms such as some combination and interaction of genes and environment rest on certain crucial assumptions which have also not been properly discussed in the political science literature so far. The rst aspect to note is the denition of environment in the twin models: Environment is all of the nongenetic external factors that inuence trait variation across a population. These inuences range broadly from the earliest biological environment of the womb, to the physical environment of a childhood house, to the social environment of the adult workplace (Alford, Funk, and Hibbing 2005, 156, emphases added; Alford and Hibbing 2008, 187; see also Plomin, Owen, and McGun 1994, 1735). With such an all-encompassing and residual delineation of the environment, the model, by denition, cannot test any substantial interaction with environmental factors. What this model and denition do is to hold everything but the genetic dierence between MZ and DZ twins as one general constant factor (as recently admitted by Smith et al. 2012, 18). This is done in order to isolate the genetic dierence between MZ and DZ twins as the genetic factor and thereby to calculate the percentage of the total trait variance that can be associated with this factor in a specic spatiotemporal environment. The causal importance of the genetic factor is then dened as that percentage, leaving interaction with the environment unspecied and, in fact, nonexistent in the model. The environment only explains the variance part that cannot be statistically associated with the genetic variable; it does not interact with the genetic component. The environment is dened in such a way that it cannot explain any part of the variance that is already associated with (or explained by) the genetic factor. The classic twin studies model is thus based on independent variables, not interacting variables, each with its correlations and separate explanatory power (see also Suhay, Kalmoe, and McDermott 2007). This separation will of course result in heritability measures that are higher than what really exists or does not exist. As Visscher, Hill, and Wray explain, Heritabilities can be manipulated by changing the variance contributed by the environment. This can be as simple as changing the method of measurement (2008, 261). One such way to obtain statistically signicant heritability measures between MZ and DZ twins is to dene the environment in this broad, residual way.
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This method is very prone to produce false-positive results of heritability estimates for all sorts of traits which are not hereditary. For example, Schonemann (1997) had shown using the National Merit Scholarship twin data that the question did you sell a used textbook during the last year? resulted in 23% heritability for men and 32% for women. The question did you have your back rubbed? was 92% heritable for men and 21% for women; and adult religious preference was 85% heritable for men and only 21% heritable for women (Schonemann 1997, 104). An additional consequence of the broad denition of the environment is that most of these studies do not dene, specify, or test distinct environments that may have aected the twins as having a certain political trait. Namely, we do not know if the twins exhibit their political traits because of or despite being aected by a particular environment. We also do not know if any two MZ twins who hold a democratic or republican political preference do so because or despite of their environment or because of their genotype (in most of the twin studies we know nothing about their genotype). This point also raises the crucial question of what exactly is an environment for having a certain political trait. It is a tricky issue to disentangle the relative weight of various possible factorssuch as family, friends, schooling, media, framing, culture, identity, domains of self-esteem, social class and income, and random events at various points of lifein dening an environment for having a certain political trait. For example, being brought up in Texas rather than in New York is not enough in itself for holding conservative views. Yet had we switched MZ and DZ twins growing up in these two states, MZ would still likely be more similar than DZ twins but could nonetheless have opposite political traits because their in-group identities and attitudes are held in contrast to positions of various perceived out-groups (Tajfel and Turner 1979; Turner 1982; Brewer and Pierce 2005). The twin studies do not and cannot test this possibility for the simple fact that it is impossible to switch or test the same pair of twins (or any individual for that matter) between political environments in which there are at least assumed opposite eects (see also Lewontin 1974, 409). The closest possible method for testing the same genotype under dierent environments is investigating the case of twins who have been separated at an early stage of childhood and have been reared apart (see the review in Bouchard et al. 2003). A greater degree of trait similarity under these circumstances may suggest that the same genotype results in similar traits despite developing under unequal environments, assuming that the upbringing environments are indeed suciently dissimilar. There are several problems with this argument, however. First, it is important to stress that the twin studies in political science have not been empirically conducted on reared-apart twins but on a comparison of MZ and DZ twins who have been reared together. None of these studies compares political traits in twins who were reared apart in environments that are as dissimilar as any two randomly chosen environments, let alone interaction of any particular genotype with dened environments. Second, a greater similarity of reared-apart MZ twins relative to DZ twins still does not specify what is an environment for having a certain political trait. The studies of twins reared apart from behavioral genetics (Bouchard et al. 1990; Bouchard and McGue 2003), which are mentioned and cited in political science in order to make the case for the validity of reared-together twin studies, do not resolve this complex issue because they also do not attempt to dene such trait-shaping environments. Third, the results of reared-apart twins showed great dierence compared with regular twin studies, and these studies are hard if not impossible to replicate in political science (Medland and Hatemi 2009, 193). The limited number of studies of twins reared apart and, no less important, the very small sample of twins participating in them (only several dozen MZ and DZ twins) greatly limit their explanatory power and make them highly prone to false positive and other confounding eects because these types of studies require samples in the thousands to have any statistical signicance. As pioneers of these studies acknowledge, Sample sizes were . . . small, and associated condence intervals were wide, suggesting the need for caution in interpreting individual correlation coecients (Bouchard and McGue 2003, 28; see also Waller et al. 1990; Martin, Boomsma, and Machin 1997, 389; Kendler 2005, 342; Medland and Hatemi 2009, 199; Benjamin 2011, 72). These limitations are not a case against studying reared-apart twins. These limitations, however, do show why relying on a few small samples of reared-apart twin studies in behavioral genetics in order to validate results of reared-together twin studies in political science (e.g., Alford, Funk, and
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Hibbing 2005, 155) is a problematic argument (see also Charney 2008a, 3034; Suhay, Kalmoe, and McDermott 2007). On top of the points above there is another cardinal issue and assumption involving the separation of causes of trait variation into genetic and nongenetic causes. The assumption is that the causes of trait variation can be broken into these independent factors, each contributing or adding separately to the outcome. The assumption that genetic and environmental causes are independent from each other and that their relative causal weight can be measured separately is known as the additivity assumption. And indeed the models employed in the twin studies are additive models in which the eects of genetic and environmental causes are measured separately from each other (e.g., Alford, Funk, and Hibbing 2005, 158; Fowler, Baker, and Dawes 2008, 2345). It is assumed that if the environment is dened and held as a constant factor, the heritability estimate discloses a genetic cause for the trait. Yet this additivity assumption greatly simplies and distorts the meaning of genesenvironment interaction, as it is currently understood in the relevant branches of biology, including behavioral genetics. This point was rst made by Lewontin, who critically noted, If an event is the result of the joint operation of a number of causative chains and if these causes interact in any generally accepted meaning of the word, it becomes conceptually impossible to assign quantitative values to the causes of that individual event. Only if the causes are utterly independent could we do so (Lewontin 1974, 402). Indeed, it is widely acknowledged in biology that it is impractical to quantify the relative contribution of genes versus the environment in the development of a specic trait because it is biologically impossible for gene and environment to operate independently of one another (Meaney 2001, 57). Biological systems are complex, non-linear, and nonadditive. Heritability estimates are attempts to impose a simplistic and reied dichotomy (nature/nurture) on nondichotomous processes (Rose 2006, 527). The scholars working in this eld are of course aware that genetic and environmental causes are not separate. For example, they note, Providing statistical estimates of the eects of genetics, shared environment, and unshared environment is not tantamount to asserting that these eects work in isolation from each other (Alford, Funk, and Hibbing 2008, 323). Fowler, Baker, and Dawes similarly admit that [s]ince the variance components are not directly observable, the ACE models assumption of additivity cannot be tested and more complicated relationships are possible. For example, it is possible that genes interact with the environment (GxE) or with other genes (GxG) to yield variation in behavior . . . (2008, 235; see also Hatemi, Byrne, and McDermott forthcoming). Yet the way that statistical associations of additive models are presented and over-claimed in political science has given the false impression that the genetic and environmental factors have been analytically separated when in reality they were not. The limitations of heritability estimates and the additive model are more known outside political science. What is more important is a derivative fatal aw of this method, which is that the genetic estimate itself actually consists of a total and complete conation of an environmental eect on random genomes for which we know nothing about. This is so because the genetic factor is dened and calculated as the degrees of trait (or phenotypic) dierences relative to the ratio of the twins genetic similarities, but the trait dierences themselves are already aected by environmental factors that have not been separated. The genetic factor therefore includes both the genetic proportion between the twin types and various random environmental eects on the expression of their traits. The method concurrently inates the heritability estimate and creates a false nature nurture partition. Put simply, environmental eects are calculated as genetic eects. Leading scholars in this eld relate to this point and explain that in a univariate model, additive genetic variance will include all the genetic inuence from all covariates, some part of geneenvironment covariation if it exists, and some part of geneenvironment interaction, if it exists (Hatemi, Dawes, et al. 2011, 74, emphases added). They also admit that this model simplies a far more complex interaction and reality (ibid.). What they apparently fail to see is that this covariation and interaction are not minor possibilities (if) or mere noise in the measurement of the genetic factor. This covariation, or rather conation, exists by denition and is built into the model because the genetic factor already includes and measures environmental eects. This point is crucial because it is at the heart of what the dened genetic factor actually measures in the twin studies.
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At minimum, it produces higher heritability estimates than real by calculating environmental eects as the genetic factor; at worse, it produces false positive results of a genetic eect where it does not actually exist.6 Heritability estimates might therefore convey the wrong notion that the heritability estimate is the amount of causal weight of the genetic factor and that this factor then interacts with the environment in whatever residual percentage of the unexplained variance. As the observation above suggests, the genetic factor is already an expression and confusion of the genetic and environmental factors. Furthermore, it is well known that a heritability estimate of 0.8 does not mean that the trait is 80% genetic and 20% environmental (Gottlieb 2003, 338; Charney 2008, 300; see also Hatemi, Byrne, and McDermott forthcoming). It merely suggests that a genetic eect may exist but says nothing about the relative importance of the genetic factor and the nature of its interaction with the environment in causing the actual trait: to what degree the genetic factor estimate of X percent for a given political trait is important, a negligible 1% or a crucial 99%; how exactly the genetic factor interacts with the environment; and how the environment aects it. This limitation is well known, but the twin study scholars in political science do not resolve these issues of relative weight and types of interaction, other than reiterating that the topic is indeed complex and requires further research. Instead, they argue that if statistical associations in the additive model disclose any role of possible genetic involvement, then genes are also likely to play a role in more complex specications (Fowler, Baker, and Dawes 2008, 235; see also Hatemi, Byrne, and McDermott forthcoming). This type of argument vastly over-claims the ndings. Similar to their limits in social science (Rustow 1970, 342; Mahoney 2001), statistical associations (or correlations) in behavioral genetics are essentially statistical claims and initial and limited tools to test hypotheses. They are not biological proofs of causation and certainly do not conrm a causal path from any set of genes to a political trait (in the context of psychiatric genetics, see Kendler 2005, 1245). Namely, even a relatively high heritability estimate does not mean that the environment does not predominantly or entirely shape any given political preference. More importantly, as I observed above, the problem runs deeper than the obvious limitations of correlations; it goes to the heart of what the genetic factor actually measures in twin studies due to the way it fuses and confuses the ratio of genetic dierences between MZ and DZ twins and their respective degrees of trait similarities (which are already aected by the environment) as a single genetic factor. Finally, the inference and explanatory limitations of association studies and heritability estimates in twin studies have also been recently acknowledged by leading behavioral geneticists who extensively employed these studies over the years. We are at a stage where scholars in behavioral genetics admit that twin studies are no longer needed precisely because no inferences can be drawn from them about the actual degree, direction, and type of genetic and environmental interactions. As Johnson, Turkheimer, Gottesman, and Bouchard have recently noted, To understand why heritability estimates are no longer important, it is necessary to understand that they are completely dependent on the specics of the samples and environmental conditions from which they are taken (2009, 217). Those pioneers of twin studies of course do not deny the role of genes in behavior but rather note that little can be gleaned from any particular heritability estimate and there is little need for further twin studies investigating the presence and magnitude of genetic inuences on behavior (ibid., 218). In this sense, twin studies and heritability estimates cannot provide the sort of explanations that are sought by political scientists interested in the complex causal relations that underlie political preferences and behavior.
Although they stress the importance of gene and environment interaction, scholars working in this field are aware that the twin study model does not actually capture this interaction on the one hand, and does not account for the possibility of such interaction and conflation in the definition and calculation of the genetic factor on the other. They admit that more advanced multivariate models are needed for this purpose and that these studies are forthcoming (Smith et al. 2012; Hatemi et al. 2011, 72). As I noted above, however, the problem and limitation of deriving conclusions on genetic effects from the method of comparing MZ and DZ twins applies to all twin study models.
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Genes for Specific Political Traits?
A number of studies have taken further steps since 2008 to identify physiological mechanisms and specic genes that may determine political traits. Oxley et al. (2008) argue that political attitudes are aected by a genetic tendency to fear; Fowler and Dawes (2008) maintain that they have identied two genes that code for voting turnout, and one gene that aects partisanship (Dawes and Fowler 2009); and Settle et al. (2010) report that a certain dopamine gene variant (DRD4-7R) seems to make a person more liberal in early adulthood if the person who carries the variant had more than six friends in adolescence. The political science scholarship has remained rather silent about such studies until now, while none of them have been replicated or validated. Oxley et al. (2008) argue that sensitivity to threat, and conservative and liberal political attitudes, involve neural activity patterns around the amygdala. Because genes aect the amygdala, they contend that political attitudes are also aected by genetic factors that aect fear. Yet the distinction between those who hold dierent political attitudes is not whether they are more or less inclined to fear, or have greater concern for the social order, but rather, that they perceive dierent things as constituting threats to that order (Charney 2009, 5). The question is to what extent a persons cognition triggers, or is triggered by, certain physical processes. Genes only code for and regulate protein production; they do not directly shape political preferences. Genes that regulate the production of testosterone, for example, may lead one to be aggressive toward conservatives or liberals, religious or secular people, men or women, one ethnic group or another, depending on ones social identity complexity and the perceived out-group in a specic context (Tajfel and Turner 1979; Brewer and Pierce 2005). The environment and cognition are major causes both in activating genes and in channeling physical processes to various and possibly opposite political ends, for the exact same genotype. Furthermore, physiologic manifestations of cognitive correlates, like electrical and chemical activity in the brain, sweaty hands, or eye blinks, do not constitute proof that a specic political trait is genetic. These physiological processes are enabled and constrained by the human genome in a broad sense, as all human traits are, but this obviously does not mean that any social or political attribute is genetically aected or heritable. The fact that the amygdala is associated with fear does not mean that it, and the genes that aect it, constitute the source of political attitudes in the brain. It has been well established that any given brain structure, including the amygdala, may have a role in various types of behaviors; and even apparent basic types of behavior and cognition depend on interactions between dierent brain structures. Just as there is no single language organ in the brain, neither will there be a single political organ in the brain (Lieberman, Schreiber, and Ochsner 2003, 6956). The argument for versions of genes that aect political behavior such as voting turnout (Fowler and Dawes 2008) and partisanship (Dawes and Fowler 2009) is based on the association of a version of a gene (allele) and a certain political trait, a method known as genetic association. The logic behind this method is that a statistical correlation between gene variants and traits may disclose some sort of relationship between the two, although genetic association does not in itself entail a causal pathway from any gene to shaping the political trait (see also Fowler and Dawes 2008, 580; Settle et al. 2010, 1195). Given the current understanding in genetics, and in light of the evidence brought forward so far in political science, the results of these studies are highly suspect of being cases of false positives and must be evaluated with great caution, as will be explained. It has been widely accepted in the last decade that the crucial majority of traits are aected by multiple genes (i.e., polygenic traits), as opposed to monogenic traits whereby a single gene aects a single trait, which is quite rare in the population (e.g., Tay-Sachs, cystic brosis). Basic traits, such as skin color, height, body weight, and disorders such as autism, diabetes, cancer, and psychiatric disorders, are known to involve many genes and genomic regions in complicated constellations, and such phenotypes are also susceptible to environmental eects (Kendler 2005). Furthermore, [s]ince the proteins produced by genes generally appear to have multiple eects, most of which we have barely begun to understand, it seems unlikely that we can be condent about all of the consequences of any particular genotype in the foreseeable future (Benjamin 2011, 68). The surprisingly low degree of genetic factors that have so far been associated with common traits and diseases
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continues to puzzle geneticists (Maher 2008, 2010; Manolio et al. 2009). Social behavior is even further complicated with a mix of various interactions and causes. Fowler and Dawes (2008, 581) also acknowledge that behavioral traits in politics are not coded in the genome and are shaped by a multitude of forces. Thus, in the context of existing theoretical and empirical research on common traits and social traits, arguments that one gene aects partisanship, two genes aect highly cognitive and environmentally sensitive political behavior such as voting turnout, and a variant of dopamine gene shapes liberal ideology are very unusual, notwithstanding the supposed controls and moderating eects of limited environmental factors. Even if genes did aect political traits, we would expect to nd far more complicated relationships. More importantly, beyond the fact that the studies have not been replicated or validated, some of these candidate genes have received rigorous review and evaluation. For example, the impact of both of the candidate genes (5-HTT gene that aects serotonin levels and the MAOA gene that aects serotonin and dopamine) that Fowler and Dawes chose to associate with political behavior, in light of earlier studies that associated them with social behavior, have been reevaluated. With regard to 5-HTT, a meta-review study revealed that research results so far are still compatible with chance ndings and that even in depression, previously assumed to be directly aected by 5-HTT, the eect is very small or negligible and the possibility that the polymorphism has no association with the disorder at all has not been excluded (Munafo et al. 2009, 216). Other research similarly concluded that the widespread acceptance of these ndings is likely to have been in part attributable to the acclaim the original article [Caspi et al. 2003] received, as well as a eld that was eager for a new approach due to the frustrating lack of progress in gene identication for mental disorders despite intensive eorts for more than a decade (Risch et al. 2009, 2469). Investigation of the association of the MAOA gene and antisocial behavior has shown mixed and conicting results (Prichard et al. 2008; Weder et al. 2009; compare with Caspi et al. 2002 and Fergusson et al. 2011; see also MAOA and depression, Huang et al. 2009). It appears that Fowler and Dawess results about the assumed connection between candidate genes and political traits are additional cases of random variations or false-positive associations, especially in light of the fact that their choice of these genes was due to those earlier studies that now lack validation (see also Hatemi, Gillespie, et al. 2011, 272). Similar nonreproducible false positives and chance ndings have been reported for dozens of traits and disorders, many of which are far more basic (e.g., physiologic) or common than political traits (Munafo and Flint 2009; Munafo et al. 2009; Risch et al. 2009; Joseph 2010). In light of the inability so far to nd and isolate the causal and predictive role of genes in physiologic traits, the challenge is likely to be at least as large for behavioral [political] traits where the causal mechanisms are arguably more complex (Benjamin 2011, 69). The neurological evidence about multiple roles of brain structures and various interacting neurological networks in the brain (Lieberman, Schreiber, and Ochsner 2003), which are clearly aected by many genes, also suggests why it is unlikely that political traits are associated with specic genes in any meaningful analytic way. Fowler and Dawess (2008) study was critically examined by Charney and English (2012) in a paper just published in the American Political Science Review. Charney and English illustrate that Fowler and Dawess ndings are indeed nonreproducible and in some cases even yield opposite results than those reported by Fowler and Dawes. Furthermore, they found several problems in the design of the study, including the specication of the phenotype (i.e., political traits); population stratication of ethnic groups; the classication of the genotype and the choice of alleles; and the lack of independence of the cases and their controls whereby, among other things, a larger proportion of MZ and DZ twins (than that which exists in the general population) was included in the sample and therefore confounded the results. It is quite uncommon at the present stage of scholarship in genetics to argue for a connection between single genes and social traits, even when supposedly controlling for moderating environmental factors. Behavioral genetics has moved away from seeking such a simple connection between genes and traits (Rose 2006; Todd 2006). Several behavioral geneticists publishing in political science have also admitted that such studies have not proven useful in terms of explanatory power and replication and that there may be no gene for a specic issue preference or ideological orientation (Smith et al. 2012, 18). Instead, they have recently oered a genome-wide approach
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that seeks to identify regions on the genome which could be associated with political traits (Hatemi, Gillespie, et al. 2011). Given the very early stage of this research, the fact that it has not been replicated, and its silence about interactions with the environment, it too lacks explanatory power about political traits and behavior (see also Charney and English 2012, 11). Furthermore, in this latter type of research it is not generally recognized that QTL [genome-wide] analysis itself relies on a prior assumption of signicant heritability (Rose 2006, 526). For example, Hatemi, Gillespie, et al. (2011) seem to assume that the political positions and lifestyles obtained in questionnaires from subjects between 1988 and 1990 could not be dierent or opposite at some earlier or later point in the subjects life or at the same time they were taken but under dierent environmental conditions. Regardless of the plausibility of this assumption, it is not what this study tests. The mapping of the genome relative to political preferences and lifestyles at one point (or points) in ones life cannot prove or even refute the hypothesis. If environmental eects changed these traits (as they often do), the associations with the chromosome regions would disappear or could even be in an opposite relationship. The contrary is also true: The lack of correlation of a trait with a specic region does not mean that such a correlation could not be established in other conditions or at a later point in time. Similar to single-candidate gene associations, though to a lesser degree, the genome-wide associations are also prone to false positives, especially regarding highly malleable characteristics such as political traits (on the genome-wide technique, see Manolio 2010). The mapping of the genome in this way also does not say how easy it is to change the political traits in question relative to the many chromosomal regions that are identied, nor does it show any interaction or moderation eects of the environment on these traits and on gene expression, eects that are known to be highly important. 5 Wider Implications
Interestingly, reports of heritability measures in twin studies are often higher for personal characteristics and political preferences than for medical disorders and other physiological traits. For example, happiness (self-reported well-being, 0.8), general intelligence and IQ (0.52 and 0.65), divorce (0.52), extraversion (0.51), neuroticism (0.46), vocational interests in adolescence (0.42), and scholastic achievements in adolescence (0.38) have higher heritability estimates than memory (0.22) and processing speed (0.22) in twin studies (McGue and Lykken 1992; Plomin, Owen, and McGun 1994, 17345; Lykken and Tellegen 1996; McGun, Riley, and Plomin 2001, 1232). Political preferences and traits show similar oddities. Martin et al. (1986) were the rst to measure heritability estimates for positions on death penalty (0.51), apartheid (0.43), censorship (0.41), white superiority (0.40), disarmament (0.38), and women judges (0.27); but oddly no less signicant estimates for positions on jazz (0.45), military drill (0.40), conventional clothes and white lies (0.35), uoridation (0.34), self-denial (0.28), computer music, teenage drivers, and learning Latin (0.26). Similarly, Alford, Funk, and Hibbing (2005, 159) reported heritability estimates of 0.41 for political positions on school prayer and property tax; 0.39 heritability for astrology; and 0.26 heritability for positions on busing, nuclear power, Democrats, and divorce; and 0.25 for positions on abortion and modern art. In striking comparison, medical disorders such as hypertension, ischemic heart disease, cancer, and Parkinsons disease have modest to negligible estimates in twin studies and none above 0.2 heritability estimates (Plomin, Owen, and McGun 1994). Clearly something is wrong about these higher heritability results for political preferences over common medical conditions. If the genes supposedly involved in the expression of political (polygenic) traits are indeed not independent of the environment, as twin study scholars admit (e.g., Fowler and Dawes 2008, 581), heritability estimates for political traits must therefore be lower rather than signicantly higher compared with the expression of biological conditions. In fact, the heritability estimates of traits in twin studies are greatly at odds with actual studies of the genome that reveal very modest to tiny eects of genes on those same traits. Whereas twin studies found heritability estimates of more than 90% for autism and more than 80% for schizophrenia, the identication of various gene variants and their associations with those traits did not yield anything close to these results, a gap which is also known as the missing heritability puzzle
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(Maher 2008, 2010; Manolio et al. 2009; Manolio 2010). Accordingly, doubts have been raised about the actual accuracy and utility of twin studies heritability estimates (Maher 2008, 21). The contrasts between the heritability estimates of common medical conditions and political positions strongly suggest that the latter are either inated or simply false positives. The alternative explanation that I have oered to the results of the twin studies in political science, thus, may have broader implications to explaining these puzzles. First, it could now be seen why comparison of twins exaggerates estimates for certain conditions. For example, a certain medical condition could appear in an MZ pair because they have a unique genotype which is responsible for it. Alternatively, the medical condition could appear in the MZ pair because they were adversely aected by the mothers condition during pregnancy or due to other environmental eects after pregnancy, despite not having that genotype (i.e., a nongenetic congenital condition). The comparison of twins cannot distinguish between the causes, and it will inate the heritability estimate by confounding and conating the environment eect as a genetic impact because MZ twins will show greater resemblance than DZ twins regardless of whether the source of the condition is genetic or due to random (nongenetic) birth problems. This may explain the gap that was noted above between the high heritability estimates of twin studies and actual genetic research. Second, twin studies can produce heritability estimates that are lower than they actually are in common traits. I will illustrate this through an examination of the Falconers formula of heritability (Falconer and MacKay 1996), which is to subtract the trait correlation of DZ from that of MZ pairs and multiply by two the resulting dierence [h (MZDZ) * 2]. Falconers formula is employed, for example, in the seminal paper of Alford, Funk, and Hibbing (2005) in political science, and well beyond.7 A genetic component for having a common physiological trait such as acne, hair loss, or one nose is likely to have very similar trait correlations in MZ and DZ twins. In such cases when correlations are similar (MZ DZ) or almost similar, the result is heritability estimates of zero (MZDZ 0, and 0 * 2 0) or low and insignicant estimates. The result implies that there is no genetic basis for these common traits when this is clearly not the case (Jerry Hirsch made a similar argument; see in Schonemann 1997, 100). Third, and most relevant to the social sciences, the alternative explanation I proposed in this paper also suggests why certain social and political traits can have higher heritability estimates than certain common traits and conditions in twin studies. This is due to the simple fact that DZ twins react more dierently to the same environmental eects compared to MZ twins. In reality, the twins can equally express opposite political preferences under dierent environments. Yet when we compare MZ and DZ twins under equal environmental impacts, this would result in emphasizing and accentuating their relative trait dierences. This explanation is consistent with, and strengthened by, the ndings that equal environments often make DZ twins growing up in the same family dierent rather than more similar to each other; and when MZ twins growing up in the same family also show dierence in their traits the reason is normally nonshared environmental factors (Plomin 1989; Plomin, Owen, and McGun 1994, 17356). Scholars who are using twin studies in political science explicitly admit this in a paper just published, where they note that MZ twins share precisely the same susceptibility to environmental inuence while the reaction of DZ twins to similar environments produce[s] variations in the phenotype (Smith et al. 2012, 28, original emphasis). What they fail to conclude, however, is that the crucial issue is not the susceptibility of any gene or genotype, but simply the obvious point that MZ will always tend to respond more alike to similar environments, no matter what they are, compared with a similar experiment with DZ twins. This explains both why political traits have such inated (and hence false) heritability estimates and why these estimates are unreasonably higher than those of certain common physiological traits and conditions.
7
Whereas there are twin studies in political science that employ different and more sophisticated methods than the Falconer formula (Medland and Hatemi 2009; Fowler, Baker, and Dawes 2008), this analysis equally applies to them because they are based on the same general method of comparing traits of MZ and DZ twins (see Smith et al. 2012).
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While many aspects of human behavior are certainly aected and shaped by genetic factors, the question remains whether twin studies actually reveal a hereditary basis of political traits. If the proposed explanation of this paper is correct, it will require rethinking the broader meaning of the twin study results, not in political science alone. 6 Conclusion and Operative Implications for Future Research
It is likely that the scholars who are working with twin studies will not agree with my alternative explanation to twin study results and that they may want to address this paper in some way. In this section I summarize the key arguments and note where they disagree with the published literature. The purpose of this section is also to focus the debate on the central issues and reduce the risk of sidetracking it into minor points. I also specify what are the operative implications for future research, at least in my view. First, the most important argument of this article is that there is indeed a biological explanation for the twin study results but it is not the explanation that has been proposed in the literature so far. I argued that MZ twins are often more alike than DZ twins because similar genomes tend to react more similarly to similar eects, no matter what these eects are and what the traits are. I made a distinction between the explanation of trait similarity (which is due to a simple genetic factor) and the completely dierent issue of explaining trait content (e.g., a political preference) which is shaped only by the environment. Given that it is a bedrock truth in biology (accepted also by those working in political science) that the exact same genotype can give rise to diverse and even opposite traits, the twin studies do not and cannot test the hypothesis that they set to prove, namely, that there is a genetic eect on political attitudes. What these studies show is that trait similarity is indeed accounted for because identical genomes tend to react similarly to a similar environment. However, scholars have been wrongly interpreting this obvious result as an indication of a genetic eect on shaping the content of political traits. The operative implication for future research is to show that in twin studies the environment is not actually the sole determinant of the trait content. Future studies need to nd a way to separate the explanation of trait similarity from that of trait content and refute this null hypothesis. As I explain above, this will not be an easy challenge but it has implications beyond political science in reference to the missing heritability puzzle that was noted above. Second, I argued that the measurements in twin studies both exaggerate the genetic eect and confound between the genetic and environmental eects. The denition of the environment in the classic twin studies leaves everything but the ratio of genetic similarity between MZ and DZ twins as a constant factor (Smith et al. 2012, 18). This research design cannot test substantial interactions with environmental factors in the degree of complexity that is known to exist in political science. The environment component only accounts for the variance part that cannot be statistically associated with the genetic variable. Furthermore, a major problem is that the genetic estimate itself actually consists of a total and complete conation of an environmental eect on random genomes for which we know nothing about. This is so because the genetic factor in twin studies is in fact the degrees of trait dierences relative to a ratio of genetic similarities, but the trait dierences themselves are already aected by environmental factors that have not been separated. This creates a false naturenurture partition. The combination of the two problems yields inated heritability estimates and false positive results. In order to demonstrate a genetic eect on political traits, future studies must nd a way to dene both the genetic factor and the environment in a more sophisticated manner and to disentangle the two separate eects. Twin studies do not appear to be the right tool for this purpose, in any statistical form, as I explained in Section 2. Third, I indicated that in twin studies the heritability measurements for political preferences (many higher than 0.4) are often more than twice those of many medical disorders and other physiological traits (many lower than 0.2). Political traits are clearly aected by multiple genes (polygenic traits). There is a wide consensus about this fact, including by scholars working to integrate biology and political science. There is clearly something suspect about the fact that heritability measures for political traits are greater than the expression of biological conditions. The analysis of the conuence of the genetic and environmental factors in twin studies may explain
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why comparison of twins exaggerates estimates for certain conditions where the source may be either genetic or environmental. I suggested (using Falconers formulae) that twin studies are prone to produce heritability estimates that are lower than they actually are in common traits where the dierences between twins are not substantial yet have a genetic source. Finally, the alternative explanation of this article explains why the twin study model is prone to yield high heritability estimates and false positive results for many political preferences that most likely do not have a genetic basis. The implication of this goes beyond political science. Solving these puzzles may also help solve the missing heritability mystery of many basic physiologic traits in biology.
Funding This research was supported by the Israel Science Foundation [grant number 297-10].
References
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Genes and Politics: A New Explanation and Evaluation of Twin Study Results and Association Studies in Political Science

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Genes and Politics: A New Explanation and Evaluation of Twin Study Results and Association Studies in Political Science

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Political Analysis (2013) 21:350367 doi:10.

Genes and Politics

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Genes and Politics

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Heritability and Environment in the Twin Studies

Genes and Politics

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Genes and Politics

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Genes and Politics

Genes for Specific Political Traits?

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Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Genes and Politics

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Genes and Politics

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Genes and Politics

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

Genes and Politics

Downloaded from http://pan.oxfordjournals.org/ at New Copenhagen University on November 12, 2013

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