Proponents of this model of drug use suggest that the consumption of pharmacological substances for medicinal purposes evolved in the backdrop of human-plant coevolution as a means of self-medication.
The hijack model of substance addiction suggests that Psychoactive drugs act on ancient and evolutionarily conserved neural mechanisms associated with positive emotions that evolved to mediate incentive behavior.
In 1953, Olds and Milner[5] published findings implicating a brain region, specifically a cluster of dopamine neurons, with reward-based learning.
[7] The hijack model of substance addiction explains that drugs that elicit positive emotion mediate incentive motivation in the nucleus accumbens of the brain.
Put another way, addictive substances act on ancient and evolutionarily conserved neural mechanisms associated with positive emotions that evolved to mediate incentive behavior.
[8] Positive emotions such as euphoria and excitation are tools chosen by natural selection to help direct the behavior and physiology of an individual towards an increase in Darwinian fitness.
Recovering alcoholics often report that the reason for relapse is often related to the impulse to compensate for negative feelings, resulting in a motivation to cope and therefore drink.
[17] Plant-derived neurotoxins are not evolutionarily novel and human neurophysiology recognizes plant toxins and activates specialized xenobiotic defenses that involve genes, tissue barriers, neural circuits, organ systems, and behaviors to protect against them.
If consumed in high enough amounts, acute nicotine toxicity can trigger failure of the respiratory system and induce death in human adults within minutes.
[17] First-time users of tobacco especially report a variety of unpleasant effects upon administration of nicotine, including nausea, vomiting, gastrointestinal distress, headache, and sweating.
[citation needed] This, when taken with the fact that nicotine is a plant toxin that evolved to deter herbivores,[20] suggests instead that the human body naturally recognizes tobacco as a toxic substance, and not a reward.
Sullivan et al. (2008)[12] has noted that humans, like other mammals, have 'inherited' the cytochrome P450 system, which functions to detoxify chemicals found in the environment, including plant neurotoxins.
[23] Similarly, in laboratory conditions, mice have been shown to moderate administration of drugs regardless of dose per injection or the number of lever presses required.
[28][9] Paleogenetic evidence suggests that the first time human ancestors were exposed and adapted to substantial amount of dietary ethanol, was approximately 10 million years ago.
The fit of allelochemicals within the CNS indicates some coevolutionary activity between mammalian brains and psychoactive plants, meaning they interacted ecologically and therefore responded to one another evolutionarily.
[17][22] Proponents of the hijack hypothesis outline a path to addiction that involves drugs co-opting neural reward systems intended for food.
Alternative mechanisms explain continued tobacco use: The majority of first time users of cigarettes report adverse reactions, including nausea, dizziness, sickness, and headache.
Given the above, opponents of the reward model of drug use suggest it is likely that a mechanism other than a false perception of an increased fitness benefit via hijacking of the brain's mesolimbic dopamine system, is leading to continued tobacco use.
Since our earliest ancestors chewed on certain herbs to relieve pain, or wrapped leaves around wounds to improve healing, natural products have often been the only ways of treating disease and injury.
In this regard, researchers have argued that the human brain evolved to control and regulate the intake of psychoactive plant toxins in order to promote reproductive fitness.
Broadly, theorists suggest that plant toxins were deliberately ingested by human ancestors to combat macroparasites (e.g. parasitic worms) and/or to ward off disease-carrying vectors (e.g. mosquitos).
Hagen and colleagues[17][22] propose that, as in other species,[34] humans began using tobacco and other plant toxins as a way of controlling infection by parasitic diseases, including helminths.
[37] Similarly, Roulette et al. (2014)[35] found in a study comparing male smoking prevalence and parasite load among Aka hunter-gatherers that treatment with commercial anthelmintics was associated with a decrease in cotinine concentrations (a measure of current tobacco use), thereby supporting their theory that humans regulate the amount of tobacco used in response to current helminth infection.
The study also found that men with higher initial tobacco use also had lower worm burdens one year later, suggesting that nicotine not only eliminates parasites, but also protects from reinfection.
[45] Research has also shown that alcohol stimulates dopamine activity in the mesolimbic-dopamine system, which amplifies the salience of natural rewards (e.g. finding food and mates) in the present environment and boost associative learning.
[52] Almost all major recreational drugs are secondary plant compounds or a close chemical analog [14] and are thus teratogenic, substances known to cause congenital abnormalities and other reproductive harms (e.g. nicotine, carbon monoxide, hydrogen cyanide).
[49] Ancestral women and conditions: In the environment of evolutionary adaptation (EEA), selection pressures shaping avoidance of or defenses against teratogenic substances would have been high.
[53] Importantly, high fertility is characterized by short inter-birth intervals, early age at first birth, and periods of breastfeeding spanning upwards of two years.
Using hepatic cells, Choi et al., (2012)[61] found that progesterone and estradiol altered drug metabolism but only when hormone concentrations reach that which is normal for pregnancy.
[62] In various studies, regular smokers have been shown to produce approximately one-third less estrogens (including estradiol) during the postovulatory menstrual phase than non-smoking counterparts.