In isolation, a single instrumental or vocal track may sound thin, but the interactions between the base, drums, guitar, and vocals form a cohesive unit and create something unique. Conducting research on the neurobiology of complex social processes is a lot like mixing on a soundboard. A single biological or psychological factor may not explain much, but interactions between these factors can provide a more comprehensive understanding of complex outcomes.


Our research on the neuropeptide oxytocin began with a study that found that higher levels of oxytocin were associated with higher rather than lower levels of relational distress. Specifically, oxytocin levels were negatively associated with the prosocial process of forgiveness and positively related to post-conflict anxiety (Tabak et al., 2011). In addition to our primary finding, we also uncovered inconsistencies in the methods research groups had been (and continue to be) using to measure oxytocin. This led to a paper about the best method of measuring oxytocin that has made a substantial impact on the field (Szeto et al., 2011). 

current research

Our lab is currently designing a follow-up study to examine how key individual differences moderate the positive relationship between relational stress and higher levels of peripheral oxytocin in blood plasma.



In our research on oxytocin, we have also examined genetic associations of oxytocin system genes. Our first study found that variation in oxytocin receptor (OXTR) gene polymorphisms were associated with increased anger and faster retaliation following a betrayal in trust (Tabak et al., 2014). This result was in agreement with our initial study of oxytocin in blood plasma demonstrating associations with negative reactions to interpersonal conflict.

Based on our previous work suggesting that oxytocin may be a biomarker of social/relational distress, we wondered whether the interaction of higher fluctuating levels of oxytocin and high levels of interpersonal distress might predict psychopathology. With colleagues at UCLA, we found that among individuals who experienced higher levels of interpersonal stress, polymorphic variation in the CD38 gene (which has been associated with higher endogenous levels of oxytocin and higher levels of social sensitivity) developed greater levels of social anxiety and depression over six years (Tabak et al., 2016). 


With colleagues from UCLA, we recently found preliminary evidence that oxytocin impairs social cognitive ability in individuals with higher levels of social anxiety (Tabak et al., in press). This suggests that higher acute levels of oxytocin may negatively affect individuals with high preexisting levels of social sensitivity. 

In a recent paper, our group also found that the effect of vasopressin on empathy is moderated by early childhood experiences in the form of paternal warmth. Specifically, among individuals who received greater levels of paternal warmth (but not maternal warmth) in childhood, vasopressin (but not oxytocin) increased empathic concern (Tabak et al., 2015). This suggests that the way fathers interact with their children may impact epigenetic modification of vasopressin (likely, AVP V1a) receptors, which can contribute to social cognitive ability later in life.


Our lab is currently designing follow-up studies to examine how specific individual differences moderate the influence of exogenous oxytocin and vasopressin on various forms of social sensitivity.


With colleagues from UCLA, our lab is currently analyzing data from a large randomized controlled trial in which participants underwent functional magnetic resonance imaging (fMRI) following administration of oxytocin or vasopressin. The goal of this project is to examine the neural effects of oxytocin and vasopressin administration while engaged in a variety of social processes. In another study that includes individuals diagnosed with social anxiety disorder and major depression, we are examining the moderating role of oxytocin system genes on neural activation while viewing aversive social stimuli.