Associations Between Sexual Desire and Within-Individual Testosterone and Cortisol in Men and Women

Abstract

Objective

The dual-hormone hypothesis (DHH) posits that some effects of testosterone on human behavior and psychology related to status-seeking are moderated by cortisol, such that they are stronger when cortisol levels are low. In support of the DHH, studies have found that cortisol negatively moderated the relationship between testosterone and such traits as status-seeking and interest in uncommitted sex. Others indicate a positive moderating influence of cortisol in some cases. Here, we test whether two psychosexual indices—sexual desire and sociosexuality—meet the expectations of the DHH in a large sample of men and women.

Method

646 women and 185 men attended lab sessions during which they provided saliva samples for hormonal analysis and responded to the Sociosexual Orientation Inventory-Revised and the Sexual Desire Inventory (180 women and 43 men returned for a second session approximately two months later). We quantified salivary hormone concentrations using ELISA and assessed within- and between-participant effects of hormones on psychosexual measures with mixed-effects models.

Results

We observed a positive interaction between within-subjects cortisol and testosterone in models of sexual desire in both men and women. For women, these effects emerged in models of general sexual desire and in models of the dyadic desire subscale and were robust to many analytical configurations. For men, the effects were limited to models of solitary desire, but were also robust to alternative analyses. We present data to quantify our risks of both type I and type II error.

Conclusions

Some of our results contrast with usual dual-hormone hypothesis predictions of negative interactions between testosterone and cortisol. We suggest several potential explanations for these results, including a positive feedback loop whereby elevated testosterone prompts increases in sexual desire and behavior, necessitating cortisol-induced mobilization of energy stores.