The richest 1% of the world’s population possesses more wealth than the rest of humanity combined, and the richest 62 people in the world possess more wealth than the poorest 3.6 billion people. The wealthy, and the institutions they finance and promote, look favorably upon research whose authors claim that such disparities are rooted in biology, and are not harmful to humanity as a whole. The wealthiest people and corporations on earth do not strive for a more equitable distribution of wealth; they want an even bigger slice of it.
There are countless obvious real-world examples showing that political policies, social struggles, and public health programs, including those involving the adjustment of income differences, lead to improved health and well-being. To cite only one example, life expectancy in France was about 45 years in 1900 (males and females combined), and almost doubled by the end of the century. In 2012, life expectancy in France was about 81 years.
Some researchers, however, argue that their findings suggest a more genetic explanation. In 2016, a group of leading behavioral genetic twin researchers and past defenders of twin research, including Matt McGue, Ian Deary, Nancy Pedersen, and Peter Visscher, published a twin study entitled “The Association between Intelligence and Lifespan is Mostly Genetic.”1 Lead author Rosalind Arden and her colleagues claimed that their twin data pointed to “common genetic effects between lifespan and intelligence,” which have “important implications for public health.” They concluded that their “results show that the relationship between lifespan and intelligence (which predicts wealth, even within advantaged families) is mostly genetic,” and called into question the environmentalist argument that policies favoring wealth redistribution and the narrowing of wealth gaps help promote human health and life expectancy. Behavioral geneticists believe that intelligence (as allegedly measured by IQ tests) is “highly heritable,” and Arden and colleagues concluded that “intelligence may mediate apparent associations between levels of education, income or occupation and morbidity and mortality.”
It is important to note that behavioral genetic researchers do not assess the importance of the environment directly. Instead, they infer the role of the environment through the controversial practice of calculating “heritability estimates,” and estimates of “shared” and “non-shared” environmental influences. Most often, these estimates are derived from twin data. Such studies are based mainly on twin pairs reared together (the “twin method”), but also on a handful of massively flawed studies of “reared-apart twins.” (These studies are supplemented by misinterpreted and misleading stories of individual reared-apart pairs reported in the media.) At the same time, behavioral geneticists usually ignore real-world refutations of their claims. To cite an additional example, which in this case relates to the “genetics of criminal and antisocial behavior” question, Australia has historically low violent crime rates despite the fact that it was founded and settled by British convicted criminals.
Evolutionary biologist Richard Lewontin criticized the behavioral genetic approach of attempting to assess the importance of the environment indirectly,
“Hereditarians claim to have the same interest as anti-hereditarians, to determine how much change is possible so that we may act rationally in social programs. But if that is really the hereditarian agenda, why do they keep studying heritability, which simple logic tells us cannot give the answer to this problem. Why do they not design studies to ask the questions about changeability directly? Because the answer would come out in the wrong direction.”2 (Emphasis in original)
Arden and colleagues’ conclusions were based in part on the indirect “variance partitioning” (model fitting) approach, where the influences of shared and non-shared environments are calculated from what is left over from twin-data derived heritability estimates. This approach is dubious even if its main assumptions are correct, but many of its key assumptions are not correct.3 Arden and colleagues acknowledged the discrepancy between real-world results, versus indirect inferences based on twin studies, when they recognized that “the claim that narrow wealth gaps promote health and life expectancy” may be true “from a broad population-level perspective.”
The researchers’ conclusions were challenged by professors Jay Kaufman and Carles Muntaner on several grounds.4 They questioned the validity of the twin method’s crucial MZ-DZ equal environment assumption (EEA), which holds that reared-together MZ (monozygotic, identical) and reared-together same-sex DZ (dizygotic, fraternal) pairs grow up experiencing roughly equal environments, and that the only factor distinguishing these twin types is their differing degree of genetic relationship to each other (100% versus 50%). In fact, the evidence shows overwhelmingly that MZ pairs’ environments are much more similar than DZ pairs’ environments. (For a critique of the EEA in twin studies of behavior, click here.) According to Kaufman and Muntaner,
“The [Arden et al.] paper makes inferences about genetics and environments, but has no direct measures of either set of variables. Rather, the key assumption on which the inference rests is the ‘equal environment assumption’ (EEA), which is that twins are not exposed to different environments based on their zygosity. This assumption is stated by the authors as a fact, but is not evaluated in these data. When evaluated in previous reports it is sometimes reported to hold approximately,and at other times found to be severely violated.”
In their response to Kaufman and Muntaner’s argument that the EEA may be “severely violated,” Arden and colleagues defended the twin method, the EEA, and accompanying heritability estimates on the basis of three extremely weak arguments:5
- Arden and colleagues’ first argument: “Concerning the equal environment assumption [EEA] in general, empirical data based on most twin studies ever published point to little or no influence of shared environmental factors on twin similarity.” In support of this position, the authors cited a 2015 twin method meta-analysis by Tinca Polderman and colleagues, which reported the combined results of 2,748 twin studies.6 In other words, Arden and colleagues cited a meta-analysis of previous twin studies—most of which assumed the validity of the EEA—in support of the validity of the EEA. Clearly, this is an illogical argument because the researchers assumed the validity of past twin studies in defense of the validity of current twin studies.
- Arden and colleagues’ second argument: “Monozygotic (MZ) twins are more likely to have more similar environments than dizygotic (DZ) twins, but this is because they create this greater similarity.” This is the “twins create their own environment” defense of the EEA, which has been used since the 1950s. It is based on an illogical circular argument, however, because the conclusion that genetic factors explain the greater behavioral resemblance of MZ versus DZ twin pairs is based on a premise stating the very same thing. Twin researchers invoking this argument cite the genetic premise in support of the genetic conclusion, and then cite the genetic conclusion in support of the genetic premise, in a continuously circular loop of faulty reasoning.7 In a 2015 review of my book The Trouble with Twin Studies, behavioral geneticist Eric Turkheimer did not dispute my argument that EEA defenses are based on circular reasoning, nor has anyone else to my knowledge.8 (See my response to Turkheimer’s predictably negative review here.)
- Arden and colleagues’ third argument: “The most comprehensive published evaluation of equal environmental similarity, based on environmental characteristics outside the twins’ control, concluded [in 2013] that the available evidence supported the validity of the assumption.” Most genetically-oriented researchers who have performed such “EEA-test” studies since the 1960s also concluded that the twin method is valid, and twin researchers’ positive evaluations of these studies have appeared since the 1980s.9 So, nothing new to report here. Yet critics have shown that this body of research is flawed on several critical dimensions, and much of it is based on the illogical arguments found in 1 and 2 above, in addition to many other faulty arguments and questionable assumptions.10
Since the 1920s, the twin method has been based on the assumption that reared-together MZ and DZ twin pairs grow up experiencing similar environments, even though most people—including most leading twin researchers—now understand that MZ and DZ environments are different. This has compelled twin researchers to concoct illogical arguments to allow them to continue their work, and authoritative social and behavioral science texts and popular media outlets continue to endorse the original twin researchers’ mistaken interpretations of their results in favor of genetics. Meanwhile, decades of attempts to uncover “genes for behavior” at the molecular level have failed to bear fruit. Turkheimer recognized in his review that “to a quite remarkable extent, it has proven impossible to find” DNA variants that influence behavioral variation, and that “scientists have not identified a single gene that would meet any reasonable standard as a ‘gene for’ schizophrenia, intelligence, depression, or extraversion.”
Kaufman and Muntaner’s letter had the virtue of compelling a group of leading genetic/twin researchers to defend the twin method’s long-controversial equal environment assumption. Like their predecessors, however, these researchers were unable to provide any valid arguments in its defense. This is an amazing development when we consider that twin method MZ-DZ comparisons provide the most frequently cited evidence in support of important genetic influences on psychiatric disorders, abnormal behavior, and common medical conditions, and twin studies in general are often cited in support social inequality and the false notion that the elites are inherently deserving of their privileged status.
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- Arden, R., Luciano, M., Deary, I. J., Reynolds, C. A., Pedersen, N. L., Plassman, B. L., McGue, M., Christensen, K., & Visscher, P. M., (2016), The Association between Intelligence and Lifespan is Mostly Genetic, Genetic Epidemiology, 45, 178-185.
- Lewontin, R. C., (1987), The Irrelevance of Heritability, Science for the People, 19, 23, 32, p. 32.
- Joseph, J., (2015), The Trouble with Twin Studies: A Reassessment of Twin Research in the Social and Behavioral Sciences, New York: Routledge.
- Kaufman, J. S., & Muntaner, C., (2016), “The Association between Intelligence and Lifespan is Mostly Genetic” [Letter to the Editor], Genetic Epidemiology, published online 3/27/2016, DOI: 10.1093/ije/dyw019.
- Arden et al., (2016), Authors’ Response to Kaufman and Muntaner [Letter to the Editor], Genetic Epidemiology, published online 3/27/2016, DOI: 10.1093/ije/dyw020
- Polderman et al., (2015), Meta-Analysis of the Heritability of Human Traits Based on Fifty Years of Twin Studies, Nature Genetics, 47, 702-709.
- Joseph, 2015. For a list of quotations from leading twin researchers using the illogical “twins create their own environment” argument in defense of the EEA and the twin method, see Appendix C of this book.
- Turkheimer, E., (2015), Arsonists at the Cathedral, PsycCRITIQUES, 60 (40), 1-4. DOI: http://dx.doi.org/10.1037/ a0039763. For my response to Turkheimer, see Joseph, J., (2015, November 2), Twin Studies are Still in Trouble: A Reply to Turkheimer, [Web log post, Mad in America “The Gene Illusion in Psychiatry and Psychology”].
- An early review of the EEA-test study literature can be found in Kendler, K. S., (1983), Overview: A Current Perspective on Twin Studies of Schizophrenia, American Journal of Psychiatry, 140, 1413-1425.
- Joseph, J., (2004), The Gene Illusion: Genetic Research in Psychiatry and Psychology under the Microscope, New York: Algora; Joseph, J., (2006), The Missing Gene: Psychiatry, Heredity, and the Fruitless Search for Genes, New York: Algora, Chapter 9; Joseph, 2015.