How do we avoid becoming sick? Several lines of evidence suggest that the emotion of disgust helps to stop us from becoming sick by reducing our contact with sources of pathogens. This function of disgust may explain why many of the things that trigger disgust particularly strongly, such as feces, rotten food, and body fluids, are sources of pathogens, and that these things trigger disgust similarly across cultures.
But why does our disgust sensitivity, the extent to which we are disgusted by typically disgusting objects, smells, or situations, sometimes change over time? One hypothesis is that, at least in women, disgust sensitivity might be tied to changes in hormone levels, and progesterone in particular, that vary over the menstrual cycle.
This progesterone-linked disgust sensitivity is thought to occur because progesterone suppresses women’s immune system. This reduced immune function might trigger behavioral responses, such as increased disgust sensitivity, to compensate. However, early studies supporting this “Compensatory Prophylaxis Hypothesis” suffered from potentially important methodological limitations. For example, they either tested only a small number of women or estimated progesterone levels, rather than measuring them directly from urine or saliva.
To address these limitations of previous research, a recent study by Benedict Jones’ research group at the University of Glasgow had three hundred and seventy-five women fill out a widely-used disgust sensitivity questionnaire (the Three Domain Disgust Scale) weekly, on up to ten different weeks. In each of these test sessions, these women provided a saliva sample, which was analyzed for the hormones estradiol, progesterone, cortisol, and testosterone.
Analyses of these longitudinal data revealed no evidence that disgust sensitivity tracked changes in women’s hormone levels. These results challenge the hypothesis that women’s pathogen disgust increases when progesterone levels are high. Jones and colleagues also found no evidence that women who had higher progesterone levels in general showed greater disgust sensitivity.
This is not the first work Jones and colleagues have published that has found little support for the hypothesis that raised progesterone triggers behaviors that function to minimize contact with sources of illness. In another recent study, they used the same type of design to investigate whether women reported greater aversions to individuals displaying facial cues of illness, such as pallor, when their progesterone levels were raised. Again, Jones and colleagues found no evidence that raised progesterone triggered illness-avoidance behaviors. Although they found that women demonstrated strong aversions to even subtle facial cues of illness, there was no evidence that the strength of these aversions was regulated by progesterone.
Of course, Jones and colleagues’ results do not rule out the possibility that some specific types of illness-avoidance behaviors that were not considered in these studies are linked to progesterone (or other hormone) levels in some women. Nonetheless, their results do suggest that progesterone-linked illness-avoidance behaviors may be less common and less pronounced than was previously thought.
These findings are described in the article entitled Hormonal correlates of pathogen disgust: testing the compensatory prophylaxis hypothesis, recently published in the journal Evolution and Human Behavior. This work was conducted by Benedict C. Jones, Claire I. Fisher, Anthony J. Lee, and Lisa M. DeBruine from the University of Glasgow, Amanda C. Hahn from Humboldt State University, Hongyi Wang from East China Normal University, and Michal Kandrik and Joshua M. Tybur from VU Amsterdam and the Institute for Brain and Behavior Amsterdam.
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