Here we develop mathematical models of the spread of self-medicative treatments for medical conditions to explore the factors that lead to treatments becoming widespread, and how a treatment's efficacy affects its rate of spread.
There is empirical support for the assumption that self-medicative treatments spread through social learning [22].
Little is known about factors affecting the prevalence of efficacious and non-efficacious self-medicative treatments.
The primary application of our models is to the spread of self-medicative treatments in humans.
Experimental evidence reveals that this can spread through social transmission, leading to the suggestion that self-medicative practices in apes are maintained as behavioural traditions [29], [30], [31].
Accordingly, while the models are developed with humans in mind, they potentially are relevant to the spread of self-medicative treatments in other animals, particularly nonhuman primates.
The gustatory cells of parasitized caterpillars fired action potentials more rapidly than those of unparasitized caterpillars in response to PA, but did not differ in their response to sucrose (a non-medicative feeding stimulant).
While several established cultural evolution models explain the persistence of maladaptive traits, none are credible alternative explanations for the existence of ineffective or maladaptive self-medicative treatments on the scale observed.
Sick chimpanzees, by contrast, do not typically engage in leaf-swallowing or another specific self-medicative behavior, bitter pith-chewing, in the absence of stress caused by parasites [4], [8].
We do not assume that observers adopt self-medicative practices according to their efficacy in treating others, since we regard this to be difficult for an individual reliably to gauge.
