We submit that genetic essentialism reflects a biased, and frequently undesirable, response to encounters with genetic information, which we will describe in more detail in following sections. However, one might question whether such responses to genetic information may instead be considered rational. Perhaps, knowing about an underlying genetic foundation for a condition should reasonably make one conclude that the condition is determined, of a specific etiology, homogenous, and natural. For example, if someone has a series of a sufficient number of repeating sequences of three bases – CAG—in the right position at the end of their chromosome 4, they will develop Huntington’s disease if they do not die prematurely of another cause. Further, the onset of their symptoms can even be predicted based on the number of repeating sequences that exist (Zoghbi & Orr, 2000). By all accounts, Huntington’s disease is determined, has a specific etiology, is homogenous, and is natural. Thinking about Huntington’s in these fatalistic ways is arguably the correct way to understand it.
However, genes influence phenotypes in different ways. On the one hand, genes can influence phenotypes through major biochemical pathways that can be measured and understood, which Turkheimer (1998) refers to as “strong genetic explanations.” This is the case with monogenic diseases and conditions that involve a small number of genes. In these cases, coming to think about them as more determined, solely caused, homogenous, and natural, as a result of learning about their underlying genetic foundation would indeed appear to be a rational response.
On the other hand, strong genetic explanation appears to be more of the exception than the rule. Monogenic diseases represent only about 2% of genetic-based diseases (Jablonka & Lamb, 2006); the norm is that multiple genes are involved, which is further complicated in that the same allele can be expressed differently depending on environmental contingencies (e.g., Caspi et al., 2002; Guo, Tong, & Cai, 2008). In summarizing the evidence for predicting disease risk on the basis of genes, Kraft and Hunter (2009) stated that “many, rather than few, variant risk alleles are responsible for the majority of the inherited risk of each common disease” (p. 1702). Genotype-phenotype relationships can be highly complex, where phenotypes emerge as the result of the interaction of many genes, when particular environmental conditions are met, and where genes may influence which environments an individual is more likely to seek out and subsequently be influenced by. Such complex relations defy a genetic essentialist response.
Turkheimer (1998) uses the expression “weak genetic explanation” to refer to those cases where a condition is known to have a genetic basis (i.e., heritability > 0), yet the mechanisms that transmit it are largely unknown or are unknowable. Much of the ways that genes relate to human conditions can be described as weak genetic explanations. Almost all human behaviors are heritable (Turkheimer, 2000), including voting behavior (Fowler, Baker, & Dawes, 2008), cigarette smoking (Kendler, Thornton, & Pedersen, 2000), and divorce (Jockin, McGue, & Lykken, 1996), although the genetic pathways underlying these are not tractable. Essentialist responses to genetic explanations for these cases are not rational – the more tenuous the link between genes and conditions, the more irrational is an essentialist response.
That genes most commonly influence phenotypes by way of weak explanations (i.e., by elevating risk assessments, increasing susceptibilities, heightening probabilities) underscores that essentialist responses to genetic associations may often be inappropriate. However, as Hinshaw and Stier (2008) argued in their account of stigma and mental illnesses, when people consider genetic attributions for a condition they frequently fail to take into account other perspectives, such as how the person fits with the environment, or how the person’s development has influenced the genesis of their condition. That is, the genetic attributions frequently get prioritized above other kinds of attributions for the phenomena. These complexities exist for most human phenomena in which nature and nurture interact. Because these complexities are more difficult to communicate and understand, it is often the case that for many people, all genetic explanations tend to be interpreted as strong genetic explanations.
In sum, we submit that when people’s genetic essentialist biases have been activated, they tend to view the associated phenomena as more immutable, homogenous, natural, and caused by relevant genetic factors than an objective analysis would suggest is appropriate. These biases lead people to attend more to the genetic causes of the phenomena at the expense of environmental, experiential, or gene-environment interactional causes. To be clear, we are not suggesting that phenomena with weak genetic explanations mean that genes are irrelevant, that the environment is the sole cause of the phenomena, or that people would fare best by viewing these phenomena as solely the product of people’s choices. Rather, we are arguing that genetic essentialist biases lead people to weigh the genetic contributions to relevant phenomena more than is justified.
As the research you quoted removed race factors, one has to wonder out-loud why you did bring it up in the first place.