Read the Outstanding Review of CRG's book, Genetic Explanations, in the Journal Logos

by jeeg 22. October 2013 22:57

Review Essay: Sheldon Krimsky and Jeremy Gruber, eds. Genetic Explanations: Sense and Nonsense (Cambridge: Harvard University Press, 2013

Fall 2013: Vol 12, No 3

It can be summed up by a quote by James Watson, who in 1953, together with Francis Crick, uncovered the molecular structure of DNA. In a 1989 interview he declared that, “We used to think that our fate was in the stars. Now we know in large measure, our fate is in our genes” [2]. Our fate is in our genes because, in the words of Richard Dawkins, “our genes have made us, body and mind” [3]. And indeed, as innumerable studies appear to have shown, what is “in our genes” is not only the cause of, or “genetic predisposition” for, almost every conceivable physical and psychological malady, but almost all complex “normal” human behavior as well. Psychologists, sociologists, anthropologists and political scientists have adopted the quantitative methodologies of the hybrid discipline of behavior genetics, and published findings purporting to show the heritability of, or a gene predisposing for, everything from voting [4] to the amount of time spent texting on a cell phone [5].

The media are enamored of claims that a given behavior is “in our genes,” and the more counter-intuitive the claim, the bigger the headline (e.g., “Too Many One-Night Stands? Blame Your Genes,” [6]; “Lost it all in the stock-market? Blame your genes” [7]). As Shirley Shalev notes, “the media play a major role in stimulating public awareness and disseminating information and conceptions about genetics in general and in particular, about the rising power of isolated genes to explain a variety of human behavior” (210). The media, however, only slightly exaggerate, and the sensationalism characteristic of media headlines is found in the titles of papers published in academic journals (e.g., “Two Genes Predict Voter Turnout” [8]). Such deterministic genetic reductionism promotes a discourse that blames behavior on genes and “a terminology that relieves or even absolves individuals of any responsibility or blame for their imperfections” (211). Indeed, such ideas have made their way into the criminal justice system:  In 2009 an Italian court reduced the sentence of a man convicted of murder on the grounds that he possessed the “aggression gene,” and hence was genetically predisposed to violence [9]. And they have fueled the rise of what Eva Jablonka calls “Genetic horoscopes,” companies such as Geneplanet, that by means of a DNA sample will enable you to “get to know everything you ever wanted to know about yourself,” including “your special talents and abilities” (71).

While the authors do an excellent job of laying out the ideology of DNA as it exists today, the bulk of the book, and by far its most important contribution, lies in the scientific debunking of this ideology. This debunking involves showing what studies of the sort “a gene causes/predisposes to/is a risk factor for trait x” have in fact found to date, and evaluating the validity of the genetic paradigm that underlies all such studies in light of advances in molecular genetics.

Jonathan Beckwith recounts the fate of several influential studies purporting to show a link between genes and criminal/anti-social behavior. In 1965, researchers reported in an article in Nature their finding that a high proportion of males in a state hospital for the mentally insane had an extra Y chromosome (i.e., were XYY males). Attempts to replicate these findings produced conflicting results until the idea of the “criminal chromosome” was finally dismissed by the original authors in 1982 (which did not stop, as Beckwith notes, James Q. Wilson and Richard J. Hernnstein from using the supposed link between XYY and criminality to support their arguments in their 1985 book Crime and Human Nature). In an influential study in 2002, Caspi and colleagues reported a link between a polymorphism (a common gene variant) of the MAOA gene, an abusive upbringing and antisocial behavior. As with the XYY chromosome, attempts at replication have been consistently inconsistent (although this association is commonly characterized as a scientific fact in psychology textbooks). As Jay Joseph and Carl Ratner note, despite all of the highly publicized claims, beginning in 2008 behavior geneticists began to acknowledge the consistent failures of replication and ultimately the failure to find a single genetic locus reliably associated with any complex behavioral traits, including intelligence, personality, and psychiatric disorders (94-95).

The situation is similar in regard to physiological – as opposed to “behavioral” – traits, although there are differences. As several of the authors note, a handful of risk factor polymorphisms have been identified, the most well-known being polymorphisms of the tumor suppressor genes BRCA1 and BRCA2 and an increased risk of breast cancer.  At the same time, as Carlos Sonnenschein and Ana M. Soto point out, cancers due to inherited genes – “inherited errors of development” – account for less than 2% of clinical cancers and only 5% of cases of breast cancer are associated with BRCA1 and 2 genes (86). In a report published in the American Journal of Human Genetics in 2012, researchers at the Harvard School of Public Health found that incorporating genetic information did not improve doctors’ ability to predict disease risk for breast cancer, Type 2 diabetes and rheumatoid arthritis above and beyond standard risk factors, including things like family history, lifestyle and behavior [10].

If “genes have made us, body and mind,” why have the particular genes been so hard to identify? As Hubbard observes, genes do not in fact “make” anything, including proteins. All of the numerous enzymes and cellular structures necessary for DNA transcription (the process of copying a segment of the DNA molecule to RNA), and for translation (the process of constructing proteins from the RNA transcripts) are external to the DNA. DNA neither “self-replicates,” nor “self-transcribes,” nor “self-translates.” Rather, the cell, in response to a host of internal and external signals, transcribes segments of DNA and translates the resulting RNAs into proteins (17-25). Nor is it the case that each gene is “coded” for a specific protein. David Moore describes how “alternative splicing” is a process in which RNAs transcribed from the same gene can be rearranged (by the cell) to produce different proteins called isoforms, something that occurs in 95% of all “protein coding” genes. Isoforms can exhibit widely divergent and even antithetical effects (47-48).

Heritability estimates depend upon the assumption that the biological causal universe can be divided between “genes” and “environment.” This is to ignore however, that genes are not the only biological agent of inheritance. Jablonka describes four non DNA-based systems of cellular inheritance, which she terms “epigenetic inheritance systems.” Included among these four are “chromatin marking” and “RNA-mediated inheritance,” two mechanisms that are part of what is commonly referred to as the “epigenome” (in a narrower sense of the term “epigenetic”) (76-80). The epigenome regulates the extent to which any given segment of DNA can be transcribed, effectively turning genes “on” and “off.” A skin cell differs from a kidney cell not because of differences in its DNA, which is presumably the same in both cells types, but because of differences in its epigenome. The consequence of a skin cell having the same genome as a kidney cell but a different epigenome is that the two cells look and act in radically different ways (i.e., have different phenotypes).  These epigenomes can be inherited because each cell type, when it divides, results in cells of the same type (e.g., skin cells only give rise to skin cells and kidney cells only give rise to kidney cells).

While the epigenome can be stable, as in cellular epigenetic inheritance, it can also be highly environmentally responsive. Mae-Won Ho describes studies in which, for example, factors such as pre- or post-natal stress can alter the epigenome, and hence, the manner in which particular genes can be transcribed. This can result in significant phenotypic differences in the absence of any changes to the DNA sequence. For example, mice raised by high stress mothers tend to exhibit, as adults, high stress behavior as well as epigenetic changes consistent with an increased stress response. Cross-fostering studies in which offspring are separated at birth and raised by “foster” mothers, consistently show that the main determinant of these changes is the rearing and not the biological mother (260-269).

The ability of the environment to “reprogram” the epigenome and thereby alter gene transcribability and phenotype is a central component of what Jablonka refers to as plasticity: “plasticity is defined as the ability of one genotype to generate different phenotypes depending on environmental cues that act as inputs on an organism’s development” (76). Plasticity can play a key adaptive role, adjusting the organism’s phenotype to the demands of its environment (e.g., in a dangerous environment, heightened stress responses can be adaptive). In sufficiently “hostile” environments (e.g., pre-natal malnutrition) plasticity can also be a cause of disease.

There is growing evidence that environmentally induced epigenetic changes can be inherited, allowing for the intergenerational transmission of acquired traits in the absence of any changes to the DNA sequence. The idea the environmentally induced changes can be inherited has long been deemed the “Lamarckian heresy,” but as Stuart Newman points out, it is now being incorporated into evolutionary theory: “evolutionary change can be “saltational” (phenotypically abrupt), rapid, and influenced by environmental change in a direct (i.e., Lamarkian fashion) and not just as a consequence of election of marginally favorable [genetic] variants” (33).

The view of DNA presented by the authors reflects current scientific understanding of the relationship between genotype and phenotype. Our genes do not “make us, body and mind.” DNA is not the sole biological inheritance. The relationship between genes and the environment is so intimate that if the environment is taken to include everything other than the DNA sequence (which would include the epigenome and the cellular environment) then the dichotomy between genes and the environment, and ultimately nature and nurture, breaks down. The environment is not a backdrop in which the developmental program, inscribed in the DNA, is activated. As Moore expresses it, “We now know that DNA cannot be thought of as containing a specific code that specifies particular predetermined (or context independent) outcomes” (47). In the words of Evelyn Fox Keller, DNA “does not even encode a program for development” (41). The idea of a predetermined code, of DNA as the rigid template of heredity in which our fates are transcribed, is at odds with phenotypic plasticity, the ability of organisms to adapt to the demands of their particular ecological niches.  This plasticity extends to the DNA molecule itself. As Stephen Talbott poetically expresses it: “The chromosome, no less than the organism as a whole, is a living, continually metamorphosing sculpture” (55).

It has been the hope of heritability and gene association studies, along with the entire mythology of DNA that they have spawned, from genetic horoscopes to MAOA criminal defenses, that we could predict and understand phenotype formation and variation solely on the basis of a person’s genotype and skip everything that intervenes between the uniting of the maternal and paternal DNA and, e.g., entering a voting booth. Such a hope – and numerous studies appear to confirm this possibility – entails that in a certain sense, all of our traits are “in our genes” (e.g., “Is There a Party in Your Gene?” – the title of a study published in Political Research Quarterly in 2009 [11], “Infidelity Might Be in the Genes” [12], “Is Empathy in our genes?” [13], “Studying Adam Lanza: is evil in our genes?” [14]).

In 1694, Nicolaas Hartsoeker produced an image of a tiny human, a homunculus, curled up inside a sperm cell. This famous image embodied the theory of “preformationism”: A human develops from a tiny, preformed human that already contains, in miniature form, all the characteristics of an adult human. Historically, “epigenesis” represented the opposing view: Humans do not develop from little preformed humans; rather, development is a process that gives rise to new and emergent structures and processes. We may smile at the naiveté of the homunculus but for the fact that today, this homunculus has been resurrected in the form of the genome, not the genome of science but a supernatural “homunculus-genome.”  What is it to say that all the features of a person are “in her genes,” but to take all the attributes of a person and ascribe them (or their “predispositions”) wholesale to what is in effect a little latent person – the inherited homunculus-genome? The reigning ideology of DNA, as an explanation as to why children resemble (or differ from) their parents, or why some people are, e.g., liberals and others conservatives, is essentially Hartsoeker’s homunculus wrapped in the language of DNA. This demonstrates the utterly regressive nature of this ideology.

This collection constitutes a potent debunking of the homunculus-genome and the ideology of DNA of which it is a part. It is an example of debunking as positive science at its best, utilizing positive science to drive out fallacious ideas. It also forces us to realize, if somewhat uncomfortably, that what needs debunking are not simply defenses of intelligent design or denials of climate change, but articles that appear in prestigious science and social science journals and are reported on in glowing terms in the science section of The New York Times.



[1]. Gould, S. J. “A Positive Conclusion,” in The Mismeasure of Man, 2nd ed. (New York: W. W. Norton, 1996), 351-353.

[2] Interview in L. Jaroff, “The Gene Hunt,” Time, March 20, 1989, 62-67.

[3] Dawkins, Richard, The Selfish Gene (New York: Oxford University Press, 1976), 21.

[4] Fowler, J.H. and C.T. Dawes, “Two Genes Predict Voter Turnout.” 2008. The Journal of Politics 70 (3):579-94.

[5] Miller, Geoffrey, Gu Zhu, Margaret J.  Wright, Narelle K.  Hansell, and Nicholas G.  Martin. 2012. “The Heritability and Genetic Correlates of Mobile Phone Use: A Twin Study of Consumer Behavior.” Twin Research and Human Genetics 15 (1):97-106.

[6] Time, December 2, 2010,   stands-blame-your-genes/

[7] Discover Magazine, February 11, 2009,

[8] Fowler and Dawes, 2008.

[9] Baum, Matthew. 2011. “The Monoamine Oxidase A (MAOA) Genetic Predisposition to Impulsive Violence: Is It Relevant to Criminal Trials?” Neuroethics:1-20.

[10] Aschard, H., J. Chen, M. C. Cornelis, L. B. Chibnik, E. W. Karlson, and P. Kraft. 2012. “Inclusion of gene-gene and gene-environment interactions unlikely to dramatically improve risk prediction for complex diseases.” Am J Hum Genet 90 (6):962-72.

[11] Hatemi, Peter K., John R. Alford, John R. Hibbing, Nicholas G. Martin, and Lindon J. Eaves. 2009. “Is There a ‘Party’ in Your Genes?” Political Research Quarterly 62 (3):584-600.

[12] Business Week, December 3, 2010,

[13] CNN Health, Nov 15, 2011,

[14] The Telegraph, April 10, 2013,


Evan Charney is Associate Professor of the Practice of Public Policy and Political Science at Duke University, and a Fellow at the Duke Institute for Brain Sciences.


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