Mind-Altering Drug Use

The use of psychoactive substances can often result in profound detriment to personal health (e.g. cancer, neurodegeneration, liver/kidney/heart failure, overdose, addiction/compulsive drug seeking at expense of self-preservation, etc.) and numerous social ills, which, prima facie, would reduce evolutionary fitness. To address this paradox of drug reward, a number of speculative evolutionary explanations exist for the prevalence of human psychoactive drug use. The "evolutionary mismatch" hypothesis, posited by Nesse and Berridge, suggests that human drug use is more likely an exaptation alongside highly sensitive neural reward circuitry that creates a strong drive for evolutionarily beneficial behaviors such as feeding and sex. They contend that drugs simply highjack circuitry designed to reward adaptive behavior, and that our widespread use of these substances reflects our unique capacity to intentionally exploit this reward circuitry (i.e. video games exploit rewards associated with hunting and fighting, junk foods exploit reward associated with evolutionarily constructed nutritional drives for high salt, fat, and sugar content, etc.). Their hypothesis is predicated on the pretense that our evolutionary landscape did not provide access to pure/potent drug, and we thus did not develop adequate defenses against their allure or adapt to avoid them due to deleterious effects.

While this hypothesis may well address prevalence of compulsive pure drug use in modern humanity, it is of dubious value for explaining the evolutionary persistence of the behavior. Not only is the hypothesis antithetical to the evolution of psychoactive phytotoxins in plants as defense mechanisms (i.e. exploitation of reward circuitry by these chemicals would encourage, rather than deter consumption), but it also neglects evidence of specific human adaptations indicative of evolution alongside psychoactive substances (e.g. population-specific cytochrome P450 polymorphisms that facilitate detoxification and degradation of regionally prevalent psychoactive compounds), and recent studies demonstrating averse responses upon first-time use of many of the most widely consumed psychoactive substances (e.g. nicotine).

Sullivan and Hagen posit an alternative hypothesis, the "deep time relationship" hypothesis, that asserts evolution of modern humans alongside psychoactive substances, and puts forth some possible evolutionary roles for their use. One such explanation is that many of these psychoactive phytotoxins occur in plants that are fairly nutrient rich but are toxic to most other species, presenting a low-demand food source to humans capable of withstanding their toxicity. Over time, this benefit may have developed into a reward response to the psychoactive substances, as they would be indicative of a valuable nutrient source that is readily available for consumption due to decreased interspecies competition. Another conjecture by Sullivan and Hagen is that the use of psychoactive chemicals, which often resemble endogenous neurotransmitters, could substitute for metabolically costly neurotransmitters and preserve some neural function when synthesis is impeded or existing supplies are depleted due to absence of dietary precursors in marginal or variable environments (akin to psychiatric self-medication). They also hypothesize that these drugs could have been used to curb maladaptive stress responses during long bouts of stress (e.g. during long hunts), or as defenses against human pathogens, such as gastrointestinal parasites. The latter function appears most analogous to drug consumption by other species. Though the evolutionary benefits of psychedelics are rather obscure due to their potentially debilitating perceptual and behavioral effects, low doses of these drugs can heighten arousal, enhance novelty detection, and increase energy, possibly enhancing capability for food-seeking or hunting. Additionally, these substances tend to structurally resemble more metabolically costly neurotransmitters, fitting well with Sullivan and Hagen's neurotransmitter-substitution hypothesis.