33. Nguyen and Ryan (2008): Table 4.
34. Walton and Spencer (2009): 1137. At low levels of prior performance, d = –0.31. At high levels of prior performance, d = –0.23. They also reported an effect size of +0.17 (the plus sign means that stereotyped students performed better than nonstereotyped students) for tests under “safe conditions that reduce threat.” (p. 1137). The study also reported results from a meta-analysis of 39 samples that included several studies of race-based stereotype threat but did not break out separate effect sizes for the race-based studies. The overall effect size, based on mean level of prior performance, was –0.48. They also reported an effect size of +0.18 for tests under safe conditions. (p. 1135).
35. The problem of unconscious researcher bias has been recognized for many decades. Simmons, Nelson, and Simonsohn (2011) pulled these arguments together and coined the phrase “researcher degrees of freedom.” The authors write, “This exploratory behavior is not the by-product of malicious intent, but rather the result of two factors: (a) ambiguity in how best to make these decisions and (b) the researcher’s desire to find a statistically significant result.” (p. 1359).
36. Stoet and Geary (2012) concluded that 11 of 20 studies that met their criteria for replications succeeded in replicating the original effect. When the sample was limited to studies that were not confounded by adjusting the results for prior test scores (see note 32), only 3 out of 10 studies replicated the original effect. Finnigan and Corker (2016) report a clear failure to replicate. Chalabaev, Major, Sarrazin et al. (2012), despite having a much larger sample, and Protzko and Aronson (2016) both failed to replicate a “self-affirmation” intervention effect that had been reported by a variety of earlier studies.
37. Lewis and Michalak (2019).
38. Stoet and Geary (2012); Flore and Wicherts (2015). The senior author of the latter study was Jelte Wicherts, a Dutch psychometrician who is one of the most highly regarded experts on all things technical about the analysis of test scores. Because so much of the controversy involves abstruse psychometric issues, I take his conclusion seriously:
To conclude, we estimated a small average effect of stereotype threat on the MSSS [math, science, and spatial skills] test-performance of school-aged girls [d = –0.22]; however, the studies show large variation in outcomes, and it is likely that the effect is inflated due to publication bias. This finding leads us to conclude that we should be cautious when interpreting the effects of stereotype threat on children and adolescents in the STEM realm. To be more explicit, based on the small average effect size in our meta-analysis, which is most likely inflated due to publication bias, we would not feel confident to proclaim that stereotype threat manipulations will harm mathematical performance of girls in a systematic way or lead women to stay clear from occupations in the STEM domain. (Flore and Wicherts (2015): 41).
39. Shewach, Sackett, and Quint (2019): 16 of 21.
40. Mueller and Dweck (1998). For a nontechnical account of subsequent literature on the dangers of praise, see Po Bronson, “How Not to Talk to Your Kids: The Inverse Power of Praise,” New York, February 11, 2007, 24–29.
41. Mueller and Dweck (1998): 33.
42. The scholarly work on growth mindset is insulated from these offshoots of the growth mindset movement. Carol Dweck and the other scholars whom I cite have no financial interest in them.
43. Sisk, Burgoyne, Sun et al. (2018).
44. Carl Hendrick, “The Growth Mindset Problem,” Aeon, March 20, 2019, aeon.co.
45. A nontechnical description of the growth mindset movement and its techniques by Carol Dweck is available online at www.nais.org/magazine. For a book-length description, see Dweck (2006).
46. For a recent full-scale description of growth mindset theory and its empirical record, see Dweck and Yeager (2019).
47. Aronson, Fried, and Good (2002); Blackwell, Trzesniewski, and Dweck (2007); Paunesku, Walton, Romero et al. (2015); Yeager, Lee, and Jamieson (2016); Yeager, Johnson, Spitzer et al. (2014).
48. Yeager, Hanselman, Walton et al. (2019).
49. Cohen (1988), Funder, and Ozer (2019).
50. Tucker-Drob, Briley, Engelhardt et al. (2016).
51. Plomin and Daniels (1987): 8.
52. Turkheimer and Waldron (2000): Table 7.
53. Turkheimer and Waldron (2000): 91.
54. Pike, McGuire, Hetherington et al. (1996).
55. Plomin (2018): 80. See also Burt, Klahr, and Klump (2015); Tucker-Drob, Briley, and Harden (2013).
56. Plomin (2018): 80.
57. John Cloud, “Why Your DNA Isn’t Your Destiny,” Time, January 6, 2010.
58. Dan Hurley, “Grandma’s Experiences Leave a Mark on Your Genes,” Discover, May 2013.
59. Israel Rosenfeld and Edward Ziff, “Epigenetics: The Evolution Revolution,” New York Review of Books, June 7, 1918.
60. Tara Swart, “Epigenetics: The Brain-Booster You’ve Never Heard Of,” Forbes, September 17, 2018.
61. Waddington (1942).
62. Nanney (1958): 712.
63. Nanney (1958): 713–14.
64. A methyl group is a carbon atom bonded to three hydrogen atoms. It is one of the commonest structural components of organic compounds.
65. This description is drawn from Dor and Cedar (2018).
66. Deichmann (2016).
67. Greally (2018): 1–2 of 2.
68. The glucocorticoid receptor is variously called GR, GCR, and NR3C1 in the literature.
69. Weaver, Cervoni, Champagne et al. (2004): 847.
70. Susser and Lin (1992), St Clair, Xu, Wang et al. (2005).
71. Tobi, Slieker, Luijk et al. (2018): 5 of 10.
72. Yehuda, Daskalakis, Bierer et al. (2016): 372.
73. “The studies included in this systematic review met the following criteria: 1) use of a case-control or cohort design; 2) use of at least one analysis investigating DNA methylation of the GR gene in response to a change or perturbation in social environment; and 3) inclusion of studies independent from one another.” Turecki and Meaney (2016): 88.
74. Turecki and Meaney (2016) has the following summary statements (pp. 91–93):
Taken together the studies “show a compelling consensus” of increased methylation in conjunction with stress in early life.
“We found multiple reports of associations between the quality of childhood experience and the methylation status of the [relevant receptors].”
“Recent evidence supports the hypothesis that epigenetic plasticity is sustained in the brain throughout adulthood, potentially as a mechanism to cope with the evolving demands of the environment; yet, there are clear moments during development when plasticity is heightened, and these may be more strongly associated with the establishment of life-long epigenetic modifications.”
“Recent rodent studies suggest that epigenetic programming of HPA function [the hypothalamic pituitary adrenal axis that constitutes humans’ stress response system] occurs at multiple levels of the HPA axis in addition to effects on hippocampal GR expression.”
“The initial reports of epigenetic regulation of hippocampal GR expression are now accompanied by reports of environmentally regulated alterations in the methylation status of multiple genes directly implicated in HPA function.”
The Turecki review also reported a variety of relationships between childhood maltreatment and characteristics of cerebrospinal fluid, cortisol levels, and other forms of sensitization of neural and endocrine responses to stress, but without relating these to changes in methylation.
Sosnowski, Booth, York et al. (2018) has the following summary statements (8–9):
11β-HSD2. “Overall, the evidence suggests an equivocal association between maternal prenatal stress and infant 11β-HSD2 methylation.”
OXTR. “Given the equivocal findings, no conclusions can be drawn regarding prenatal stress and infant OXTR methylation.”
SLC6A4. “To date, the findings provide no conclusive evidence that maternal prenatal stress is a
ssociated with variable infant SLC6A4 methylation.”
CRH, CRHBP, and FKBP5. “Overall, the evidence linking prenatal stress and methylation of these genes is limited, but given the significant findings, further examination of each gene is warranted.”
The Sosnowski review also reported the results of four epigenome-wide association studies (EWAS). EWAS is analogous to GWAS, but for the epigenome instead of the genome. One of the four EWAS found 3,405 genes with infant methylation that were statistically associated with maternal prenatal stress, but none of them were in the HPA axis. Two of the four found no effects of maternal depression or psychotropic medication on infant DNA methylation. EWAS studies have the advantage of being hypothesis-free. The fourth study found 42 such associations, but 33 of them revealed decreased levels of infant DNA methylation. None of them were located within the HPA axis. Sosnowski, Booth, York et al. (2018): 6. These studies cannot be treated as strong disconfirmation of a role for methylation in the HPA—the sample sizes were too small for that—but they fail to support the findings of the candidate gene studies.
75. This is a common paraphrase of Max Planck’s original version: “A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.” It was made famous by Kuhn (2012): 150.
76. Greally (2015).
77. Kevin Mitchell, “The Trouble with Epigenetics (Part 1),” Wiring the Brain, January 7, 2013, wiringthebrain.com; Kevin Mitchell, “The Trouble with Epigenetics (Part 2),” Wiring the Brain, January 14, 2013.
78. Kevin Mitchell, “Grandma’s Trauma—A Critical Appraisal of the Evidence for Transgenerational Epigenetic Inheritance in Humans,” Wiring the Brain, May 29, 2018, wiringthebrain.com.
79. Jill Escher, “No Convincing Evidence? A Response to Kevin Mitchell’s Reckless Attack on Epigenetic Inheritance,” Germline Exposures, July 18, 2018, germlineexposures.org.
80. Kevin Mitchell, “Calibrating Scientific Skepticism—A Wider Look at the Field of Transgenerational Epigenetics,” Wiring the Brain, July 22, 2018, wiringthebrain.com.
81. Perez and Lehner (2019).
82. Perez and Lehner (2019); Waterland and Jirtle (2003).
83. Kazachenka, Bertozzi, Sjoberg-Herrera et al. (2018).
84. Yeager (2019).
85. Yeager (2019).
86. Horsthemke (2018). The author is the director of the Institut für Humangenetik at the University of Duisburg-Essen. Here is his account of “the roadmap to proving transgenerational epigenetic inheritance” on pages 2 and 3 of 3:
1. Rule out genetic, ecological and cultural inheritance. For studies in mice and rats, inbred strains and strictly controlled environments need to be used. When a pregnant female animal is exposed to a specific environmental stimulus, F3 offspring and subsequent generations must be studied in order to exclude a direct effect of the stimulus on the embryos’ somatic cells and germ cells. Even more desirable is the use of in vitro fertilization (IVF), embryo transfer and foster mothers. When a male animal is exposed to an environmental stimulus, F2 offspring must be studied in order to exclude transient effects on germ cells. To ensure that any phenotype is exclusively transmitted via gametes, IVF must be used, controlling for possible artifacts relating to IVF. In contrast with laboratory animals, it is impossible to rule out ecological and cultural inheritance in humans, but genetic effects should and can be excluded. If an epimutation apparently follows Mendelian inheritance patterns, be cautious: you are more likely looking at a secondary epimutation and genetic inheritance. Study the haplotype background of the epimutation: if in a given family it is always on the same haplotype, you are again most likely dealing with a secondary epimutation. Do whole genome sequencing… to search for a genetic variant that might have caused the epimutation and be aware that this variant might be distantly located. Good spots to start looking are the two neighboring genes, where a mutation might cause transcriptional read-through in sense or antisense orientation into the locus under investigation. Unfortunately, if you don’t find anything, you still cannot be 100% sure that a genetic variant does not exist.
2. Identify the responsible epigenetic factor in the germ cells. Admittedly, this is easier said than done, especially in female germ cells, which are scarce or unavailable. Be aware that germ cell preparations may be contaminated with somatic cells or somatic DNA. Use swim-up (sperm) or micromanipulation techniques to purify germ cells to the highest purity. Exclude the presence of somatic cells and somatic DNA by molecular testing, for example by methylation analysis of imprinted genes, which are fully methylated or fully unmethylated only in germ cells.
3. Demonstrate that the epigenetic factor in the germ cells is responsible for the phenotypic effect in the next generation. If possible, remove the factor from the affected germ cells and demonstrate that the effect is lost. Add the factor to control germ cells and demonstrate that the effect is gained.… In light of [the problems of doing such experiments in humans], this might currently be too much to ask for to prove transgenerational epigenetic inheritance in humans, but should, nevertheless, be kept in mind and discussed.
Despite some unfamiliar technical language, enough of Horsthemke’s description of the roadmap is comprehensible to a layperson to convey a sense of how difficult proof is going to be. Much of the roadmap also applies to the requirements for proving epigenetic effects within a generation among humans. It seems safe to conclude that the gap between what has actually been accomplished to date and what has been conveyed to the public is enormous. As for a technical pronouncement about the state of knowledge, here is Horsthemke’s closing paragraph:
In conclusion, in my opinion, even if the molecular mechanisms exist to transmit epigenetic information across generations in humans, it is very likely that the transgenerational transmission of culture by communication, imitation, teaching and learning surpasses the effects of epigenetic inheritance and our ability to detect this phenomenon. Cultural inheritance has certainly had an adaptive role in the evolution of our species, but the evidence for transgenerational epigenetic inheritance, as laid out above, is not (yet) conclusive. For now, I remain skeptical.
87. I am referring to the phenomenon known as regression to the mean. It is a statistical phenomenon that applies far beyond heritable traits. See Humphreys (1978).
Part IV: Looking Ahead
1. Wilson (1998): 269.
14: The Shape of the Revolution
1. “Orders of magnitude” is often misused. In this case, it is the correct descriptor. The mainframe used by Mission Control for the moon landing in 1969 was IBM’s most advanced model. It had one megabyte of storage.
2. Risch, Spiker, Lotspeich et al. (1999): 504.
3. Boyle, Li, and Pritchard (2017): 1177.
4. Boyle, Li, and Pritchard (2017): 1177.
5. Boyle, Li, and Pritchard (2017): 1179.
6. This number refers to the Boyle study but is given in Jordan, Verbanck, and Do (2018).
7. Davies, Lam, Harris et al. (2018).
8. Pickrell, Berisa, Liu et al. (2016): 709–10.
9. The terminology and example are taken from Jordan, Verbanck, and Do (2018), though the concepts originated earlier.
10. Jordan, Verbanck, and Do (2018).
11. Graham Coop, “Polygenic Scores and Tea Drinking,” The Coop Lab, March 14, 2018, gcbias.org.
12. Coop, “Polygenic Scores and Tea Drinking.”
13. Allegrini, Selzam, Rimfeld et al. (2018).
14. Plomin (2018): vii.
15. Plomin (2018): 137.
16. The following discussion is taken from Plomin (2018): 161–77.
17. Plomin (2018): 165.
18. Plomin (2018): 166.
19. Plomin (2018): 170.
20. Turkheimer (2011).
21. Turkheimer’s article was one of the commentaries on the 30th-anniversary republication (of Plomin and Daniels (1987)). Plomin (2011)
.
22. Turkheimer, Pettersson, and Horn (2014): 532.
23. Johnson, McGue, Krueger et al. (2004).
24. McGue and Lykken (1992).
25. Turkheimer, Pettersson, and Horn (2014): 532.
26. Feldman and Ramachandran (2018). The phrase in quotes is taken from Lewontin (1974).
27. Turkheimer (2011): 600.
28. Plomin (2018): 162.
29. Trzaskowski and Plomin (2015). For an example of its application, see Trzaskowski, Harlaar, Arden et al. (2014).
30. For the position of the advocacy school, see Scheper-Hughes (1995) and Angel-Ajani and Civico (2006). For an account by an anthropologist with a traditional perspective, see Glynn Custred, “Turning Anthropology from Science into Political Activism,” James G. Martin Center for Academic Renewal, February 17, 2016, www.jamesgmartin.center. In 2010, the executive committee of the American Anthropological Association, the discipline’s major professional association, dropped the word “science” from its mission statement. See Nicholas Wade, “Anthropology a Science? Statement Deepens a Rift,” New York Times, December 9, 2010.
31. The titles of those that I classified as directly involving sex were: “The Mark of a Woman’s Record: Gender and Academic Performance in Hiring”; “Precarious Sexuality: How Men and Women Are Differentially Categorized for Similar Sexual Behavior”; “Unemployment, Temporary Work, and Subjective Well-Being: The Gendered Effect of Spousal Labor Market Insecurity”; “Policy Generosity, Employer Heterogeneity, and Women’s Employment Opportunities: The Welfare State Paradox Reexamined”; “Is There a Male Marital Wage Premium? New Evidence from the United States”; “The Evolution of Gender Segregation over the Life Course”; and “Women in the One Percent: Gender Dynamics in Top Income Positions.” The ones I classified as directly involving ethnicity were: “Sharing the Burden of the Transition to Adulthood: African American Young Adults’ Transition Challenges and Their Mothers’ Health Risk”; “Firm Turnover and the Return of Racial Establishment Segregation”; “Compounding Inequalities: How Racial Stereotypes and Discrimination Accumulate Across the Stages of Housing Exchange”; and “The Paradox of Persistence: Explaining the Black-White Gap in Bachelor’s Degree Completion.” The ones I classified as directly involving class were: “Social and Genetic Pathways in Multigenerational Transmission of Educational Attainment”; “Income Inequality and Class Divides in Parental Investments”; “Education, Smoking, and Cohort Change: Forwarding a Multidimensional Theory of the Environmental Moderation of Genetic Effects”; “Relative Education and the Advantage of a College Degree”; “Political Consequences of Survival Strategies Among the Urban Poor”; “Educational Inequality, Educational Expansion, and Intergenerational Income Persistence in the United States”; and “Encultured Biases: The Role of Products in Pathways to Inequality.”
Human Diversity Page 59
