In our study “Prejudice and truth about the effects of testosterone on bargaining behaviour” we have shown that individuals with exogenously increased testosterone levels make significantly more fair bargaining offers in the ultimatum game compared to subjects who received a placebo. However, subjects who believed that they received testosterone— regardless of whether they actually received it or not—behaved much more unfairly than those who believed that they were treated with placebo. Finally, we found no effect of testosterone administration on the responder’s rejection behaviour. This finding appears to be challenged by findings of Zak et al., who report a decrease in proposer offers and a decrease in generosity after testosterone administration. Before we respond to the particulars of the comment by Paul Zak, we would first like to point out an important statistical issue in the Zak et al. paper.

Zak et al. used a sample of 25 subjects in a “within-subjects” design, i.e. each subject played the ultimatum game 8 times. They played the game 4 times in the testosterone condition and 4 times in the placebo condition. Thus Zak et al. recorded a total of 200 decisions.

In the statistical analysis one has to take into account that these 200 decisions are not independent of each other and that there are only 25 independent observations. In their statistical analysis however, Zak et al. assume that the 4 decisions of each individual in the two treatments are independent of each other. This assumption is clearly not justified and tends to inflate the statistical significance of the results.

Zak et al. sent us their raw data for a re-analysis. Based on the dataset we received, we conducted the t-test in a way that only assumes 25 independent observations by comparing each subjects’ average generosity between the testosterone and placebo treatment. We found that their main result that subjects under Androgel are less generous than under placebo is no longer significant (paired t-test, p = 0.33, two-tailed, n = 25). Thus, based on a proper statistical test, the null hypothesis of no treatment group differences between the placebo and the Androgel condition cannot be rejected.

In addition, we have the following response to the comment by Paul Zak.


Study design.

The decision to choose a “between” or a “within” subjects design is largely dependent on the research question and there is not simply a good and a bad choice. Virtually all social decision making studies employ “between” subjects designs, because “within-subjects” designs may carry the risk of spill-over effects across the treatment conditions. Such spill-over effects were noted by Zak et al. who found a significant increase in proposer offers across the two treatment sessions. This might explain the unusually high average offer of above 50% in the placebo group, which has hitherto never been observed in Western societies (Henrich et al., 2006). On the other hand, the costs of choosing a ”between” subjects design is the relatively lower statistical power, which we counteracted with a relatively larger sample size.


Administration procedure and blood levels.

Blood measures verify whether one is successful in exogenously increasing testosterone levels. We did not take blood measures during our experiment because the use of syringes may have stressed the subjects. This might be accompanied by a cortisol response which obviously might interact with the testosterone administration. But even without such a neuroendocrine response, subjects nevertheless could have changed their behaviour. However, we are confident that we increased levels of testosterone, because our testosterone administration procedure is well-established and robust pharmacokinetic data have been published previously (Tuiten et al., 2000). We used the same dosage, route of administration and a subject pool that has the same age range, gender and other important communalities with the sample used by Tuiten et al.

Our procedure of testosterone administration contrasts with the one used by Zak et al. because in the latter case no data support the reliability of the method. In particular, as testosterone levels tend to be higher in the morning and lower in the evening, blood measures should be taken at the same daytime. Despite this fact, Zak et al. took the first (baseline) blood-draw in the evening and the second one in the early morning. Therefore, one cannot rule out that their reported increase in testosterone levels after gel administration was entirely due to the natural circadian fluctuations in serum testosterone.


Beliefs about the drug.

The community now becomes increasingly aware that preconceptions (“beliefs”) about drugs are potent determinants of behaviour. These may take the form of the well-known placebo or nocebo-effect. Because social decision making is sensitive to framing effects and expectations, any preformed belief about potential effects of a drug could interfere with the outcome measure. This fact can have far-reaching consequences: if subject‘s beliefs about a substance cause them to act in favour of the true effect of the substance itself, the substance effect might be overestimated. On the other hand, if subjects’ beliefs about a substance causes them to act against the true effect, as it is the case in our study, we are likely to underestimate the true effect of the substance. Although our measure of the beliefs is not perfect, which we extensively discuss in the paper (on page 358, left column), our observation that beliefs are highly negatively correlated with bargaining offers teaches us an important methodological lesson, which will likely influence future study designs.


Neurobiological mechanisms.

The identification of the neurobiological mechanisms by which testosterone may influence social behaviour is obviously one of the major challenges in the field. Both Eisenegger et al. and Zak et al. do not address these research questions. Future research, in particular animal research, will have to provide models of how hormonal drug challenges affect neurobiological processes and how these translate back into behaviour. So far, animal research has suggested many different potential mechanisms, including for example through the aromatisation of testosterone to estradiol, which acts on estrogen receptors in the amygdala, through a down-regulation of oxytocin receptors and/or an up-regulation of vasopressin receptors or by changing catecholamines and/or serotonin neurotransmission. Thus, we are reluctant in attributing testosterone administration effects to one single neurobiological mechanism in humans.