Oxytocin Receptors and Empathy: Neuroethics Journal Club

This week, the Core’s journal clubbers discussed a paper by Sarina Rodrigues et al., entitled “Oxytocin receptor genetic variation relates to empathy and stress reactivity in humans.” The abstract follows:

Oxytocin, a peptide that functions as both a hormone and neurotransmitter, has broad influences on social and emotional processing throughout the body and the brain. In this study, we tested how a polymorphism (rs53576) of the oxytocin receptor relates to two key social processes related to oxytocin: empathy and stress reactivity. Compared with individuals homozygous for the G allele of rs53576 (GG), individuals with one or two copies of the A allele (AG/AA) exhibited lower behavioral and dispositional empathy, as measured by the “Reading the Mind in the Eyes” Test and an other-oriented empathy scale. Furthermore, AA/AG individuals displayed higher physiological and dispositional stress reactivity than GG individuals, as determined by heart rate response during a startle anticipation task and an affective reactivity scale. Our results provide evidence of how a naturally occurring genetic variation of the oxytocin receptor relates to both empathy and stress profiles.

Our discussion focused on how best to interpret the findings. What can we really conclude from the correlation discovered in this study? Can we claim to have knowledge of “a gene for empathy” now? If not, what can we reasonably say about why some people are more empathetic than others?

trust me

How much does "liquid trust" affect you?

Initially, one observer pointed out that the parse on “empathy” employed by the study does not necessarily match up with more familiar folk understandings of what empathy means. There is no reason to suppose that a rather cruel and manipulative kind of person, for instance, would not score high on the “Reading Mind in the Eyes” Test – the ability to carefully and accurately intuit others’ affective states being a skill essential to success in waging emotional warfare.

Still, let us suppose that “empathy” has some unitary behavioral referent that we can all agree upon. The interesting question is what a person’s oxytocin receptor genotype necessarily indicates about that behavioral phenotype. We are familiar with the temptation to say that the answer is “everything – the trait is completely determined by the gene.” However, the paper responsibly cautions (though not until near the end) against this interpretation, and such caution has trickled through to popular science media: cf. Eurekalert including head author Sarina Rodrigues’ well-chosen words:

However, Rodrigues cautioned against drawing too many conclusions just yet from the study’s findings. She said these population trends should not be translated to individuals, meaning there are plenty of people in the AA or AG gene pool who are empathetic, caring individuals.

“I tested myself and while I am not in the GG group, I’d like to think that I am a very caring person with empathy for others,” she said. “These findings can help us understand that some of us are born with a tendency to be more empathic and stress reactive than others, and that we should reach out to those who may be naturally closed-off from people because social connectivity and belongingness benefits everyone.”

Our journal club noted that this modest approach need not be viewed as some counter-intuitive restraint on the “natural” interpretation of the study results; rather, it falls right out of the data. The results basically identify non-identical bell curves of empathy levels in genetically different populations – groups that differed to a statistically significant degree. But nowhere is it claimed that these bell curves are non-overlapping. Far from it! Individuals falling on the right-hand fringe of the A-group will still be vastly more empathetic than those falling on the left-hand fringe of the G-group. Hence to think of the “genetic determinist” interpretation of Rodrigues et al’s results as reasonable is just to forget or suppress your grasp of basic statistics. It is akin, conceptually if not morally, to assuming that an individual member of an ethnic group must conform to an ethnic stereotype.

For our group, the most interesting topic of discussion was this: it might seem that our deflationary view of the study’s results vindicates a holistic, philosophical approach to understanding genes and phenotypes – particularly one couched in the language of the humanities. “We cannot understand what makes a person empathetic simply by examining their genome,” our token philosopher might say. “Rather, we must look to the totality of interpersonal relationships, cultural influences, social norms, and practical-rationality structures that have suffused the individual’s lifeworld.” (Forgive my awkward rendition; I am not a student of this type of philosophy, and that is an honest attempt at taking its perspective, not a tongue-in-cheek caricature.) As the above analysis suggests, there is considerable wisdom to at least the negative claim (“we cannot understand x simply by z-ing”) here.

What our resident scientists took issue with, however, was the assertion of the further positive claim (“we can/should understand x, rather, by w-ing”) without hard evidence, or, worse, with the attitude that the claim is exempted from the tribunal of hard evidence. Presumably, the influence of an individual’s personal relationship history on their capacity for empathy is scientifically tractable. (Maybe, as some of us suggested, it would make for better, more airtight science to find a reliable neurobiological proxy for “the influence of an individual’s personal relationship history.”) If that is indeed the case, then its effect deserves to be measured, so that we can judge the viability of the philosopher’s alternative explanation.

I would be remiss, as a philosopher who inclines toward the analytic tradition, to allow the impression that all philosophical involvement in the natural sciences looks like the above case. Some philosophy of science/ of biology makes explicitly evidential claims – generally citing extant scientific research as backup. Other times, naturalistic philosophers make claims that I will call properly non-evidential. Rather than spill endless ink on what that means, I direct those interested in the topic to a fantastic paper by Dupré and Goldsmith, entitled “Are whales fish?” It can be found in Folkbiology, MIT Press, Cambridge, Ma. and London (1999) pp. 461–476.


5 thoughts on “Oxytocin Receptors and Empathy: Neuroethics Journal Club

  1. Pingback: Oxytocin Receptors and Empathy: Neuroethics Journal Club … | Empath Intelligence Blog

  2. Hi Roland,

    Great post! Your assessment of what the phenomenologically-inclined thinker might say about genetic determinism seems quite accurate to me. But I submit that we need not have recourse to phenomenology as such to reject genetic determinism. As scholars like Lewontin (himself a population biologist), EF Keller (philosophy of science), and Jeremy Freese (sociology) have all pointed out in one way or another, genetic determinism is on its face incoherent because genes do not by themselves determine anything at all. Genes only express as part of an inordinately complicate set of nonlinear dynamical systems, with hundreds if not many thousands of different variables that interact with each other to produce system behavior. Thus, pointing out some kind of genetic linkage with, say, empathy, is to my mind exceedingly uninteresting because what really matters is how genetic information expresses in ways that affect the presence of lack thereof of empathy. And that latter inquiry is, of course, significantly more complicated, and cannot remotely be sealed off from social, environmental, and cultural factors.

    Keller goes so far in her book on the gene to expressly argue that the concept of “gene” is neither precise nor particularly useful, but its inordinate metaphorical power to confuse and mislead recommends that it be retired (she is not, I think, decrying the fact that it is a metaphor, but is rather suggesting that we should be careful about which metaphors we utilize and rely on so much).

    Concerns like this, among others related to my central area of research and interest (the social determinants of health), suggest to me the oft-cited distinction between biology and society is facially incoherent. There is no such thing as biological effects, let alone of human behavior, that somehow exist in some presocial or nonsocial state. We are social beings, and as Nancy Krieger as eloquently stated and shown, our social lives and the lives of our social networks even before we are born are imprinted on our bodies and our health patterns.

    To my mind, none of this implies that the study of empathy is not amenable to exposition via the methods of the “hard sciences.” What it does imply is that the notion that genetic linkages have much explanatory power separate and apart from analysis of the social, environmental, and cultural factors that shape their expression is implausible, to say the least.

  3. Thanks, Daniel – I definitely agree with you that there’s all manner of philosophical angles from which to resist genetic determinism. I’m particularly familiar with the philosophy of biology approach – my exposure to it as an undergrad involved a lot of Dick Lewontin, in fact. I actually recall writing a term paper I liked a lot, on why the notion of a genetic “code” is incoherent (there’s no defensible understanding of “code” on which genes “code” for proteins, and even mRNA triplets don’t always “code” for amino acids).

    While I am not fully on board with the idea that there’s nothing at all to the distinction between biological and (broadly speaking) non-biological factors, I definitely appreciate the case against it being some kind of deep, crystal-clear, a priori conceptual fault-line.

  4. Pingback: Ripple Effect #2 —Oxytocin Recptor can trigger empathy and listening « The Wick

Comments are closed.