First, it is unclear that Müller & Schumann's (M&S's) model of drug instrumentalization is necessarily an evolutionary argument. In their rationale for drug use as an adaptation, M&S state that “non-addictive psychoactive drug instrumentalization helps to solve an adaptational problem, employing species-general learning mechanisms that dynamically adapt the search for and consumption of plants and plant compounds” (sect. 4.1, para. 4). However, a domain-general cognitive model, which is what M&S are invoking here, does not require an evolutionary argument for a specific suite of behaviors like drug use – such a mechanism can putatively “solve” contextual problems based on trial-and-error learning. Note that similar arguments supported by empirical data have been made for functional situational exploitation of psychoactive drugs, without invoking adaptationist theory (e.g., Sahakian & Morein-Zamir Reference Sahakian and Morein-Zamir2007).
Other aspects of M&S's adaptationist hypothesis strike us as implausible. Psychoactive drugs have their effects because they alter neural signaling, often by mimicking neurotransmitters such as acetylcholine or dopamine, or by interfering with their metabolism or reuptake. Consider two evolutionary scenarios: (1) the evolution of a complex neurobiological mechanism to manipulate the central nervous system via untargeted systemic administration of environmental neurotoxins, which then accurately evaluates the social consequences of the resulting behavioral consequences, as M&S propose; or (2) the evolution of pathways to directly modulate endogenous neurotransmitter signaling systems in the CNS in response to social cues in the environment. We find (2) more plausible because it provides the same benefits as (1) but avoids its manifold costs.
To be clear, we believe that there might be adaptations to manipulate one's own CNS with plant neurotoxins, but only in circumstances, such as mental illness or nutritional deficiency, in which the brain would be unable to adequately modulate endogenous neurotransmitter signaling (Sullivan & Hagen Reference Sullivan and Hagen2002). We and others have also argued that plant neurotoxins could provide non-cognitive benefits, such as combating rapidly co-evolving pathogens (Hagen et al. Reference Hagen, Sullivan, Schmidt, Morris, Kempter and Hammerstein2009; Sorensen-Forbey et al. Reference Sorensen-Forbey, Harvey, Huffman, Provenza, Sullivan and Tasdemir2009; Sullivan et al. Reference Sullivan, Hagen and Hammerstein2008).
Second, M&S have proposed a range of new or novel adaptive behaviors associated with drug use without considering how they might negatively affect existing cognitive mechanisms. For example, M&S propose that people may use drugs for “improved social interaction” (sect. 4.2.1). Primates are characteristically “social” and can be assumed to have cognitive adaptations to facilitate sociality and attention. One must assume that natural selection has “shaped” those adaptations to perform well on average. Any drug that affects the nervous system is also going to interfere with the existing primate mechanisms for sociality. How do we, or M&S, know that this interfering with the primate nervous system is going to improve or impair the existing mechanisms for sociality? M&S seem to have given this little thought, and their account is somewhat naïve in that no reference is made to the possibility of drugs causing impairment in social cognition. After all, there is overwhelming evidence that drugs such as alcohol interfere with other cognitive mechanisms, such as those involved with motor control.
M&S reiterate this theme in their proposal that drug use increases sensory curiosity and expands perceptual horizon. Given that all mammals have evolved senses, perception, and attention to survive and reproduce in their various environments, how is interfering with these existing mechanisms an adaptation? M&S do not address the possibility of impairing existing sensory adaptations. Again, their accounts seem somewhat hopeful at best.
Third, we disagree with M&S's characterization of our notion of “the paradox of drug reward.” Our idea is that there is a conflict between the evolutionary biological view that plant toxins evolved to deter animal herbivores, and current proximate neurobiological models that argue that commonly used drugs (which are also plant toxins or their close chemical analogs) are rewarding in animal nervous systems. M&S propose that the “‘paradox of drug reward’ may be resolved at the dose-response level: In a low- to medium-dose range, the drug effect is not toxic in the sense of being an immediate threat to life. In the range of medium to low doses, therefore, a role for drugs in functional adaptation can reasonably be considered” (sect. 2, para. 2). We do not disagree with the latter part of M&S's statement, at least, but we are unclear what it has to do with the paradox. M&S seem to be saying that the “goal” of the toxin-bearing plant is to kill the herbivore, whereas functional benefits may occur at the sub-lethal dosage. Here M&S appear to have made the Spencerian “survival of the fittest” error with the presumption that evolution requires lethal selection. In reality, chemical defenses in plants are more likely to interfere with herbivore feeding and reproduction, not to kill them, and the dosage that will achieve this is different for insects and mammal herbivores in their respective ecological niches. The possible range of chemical defense dosages from wild plants indeed allows the possibility of functional benefits for invertebrates and vertebrates, as we have previously argued and outlined in great detail in the papers that M&S cite.
Finally, M&S include a section on the implications of their model for drug policy (sect. 7). In our view, M&S's ideas need development, and it is premature to make policy recommendations.
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First, it is unclear that Müller & Schumann's (M&S's) model of drug instrumentalization is necessarily an evolutionary argument. In their rationale for drug use as an adaptation, M&S state that “non-addictive psychoactive drug instrumentalization helps to solve an adaptational problem, employing species-general learning mechanisms that dynamically adapt the search for and consumption of plants and plant compounds” (sect. 4.1, para. 4). However, a domain-general cognitive model, which is what M&S are invoking here, does not require an evolutionary argument for a specific suite of behaviors like drug use – such a mechanism can putatively “solve” contextual problems based on trial-and-error learning. Note that similar arguments supported by empirical data have been made for functional situational exploitation of psychoactive drugs, without invoking adaptationist theory (e.g., Sahakian & Morein-Zamir Reference Sahakian and Morein-Zamir2007).
Other aspects of M&S's adaptationist hypothesis strike us as implausible. Psychoactive drugs have their effects because they alter neural signaling, often by mimicking neurotransmitters such as acetylcholine or dopamine, or by interfering with their metabolism or reuptake. Consider two evolutionary scenarios: (1) the evolution of a complex neurobiological mechanism to manipulate the central nervous system via untargeted systemic administration of environmental neurotoxins, which then accurately evaluates the social consequences of the resulting behavioral consequences, as M&S propose; or (2) the evolution of pathways to directly modulate endogenous neurotransmitter signaling systems in the CNS in response to social cues in the environment. We find (2) more plausible because it provides the same benefits as (1) but avoids its manifold costs.
To be clear, we believe that there might be adaptations to manipulate one's own CNS with plant neurotoxins, but only in circumstances, such as mental illness or nutritional deficiency, in which the brain would be unable to adequately modulate endogenous neurotransmitter signaling (Sullivan & Hagen Reference Sullivan and Hagen2002). We and others have also argued that plant neurotoxins could provide non-cognitive benefits, such as combating rapidly co-evolving pathogens (Hagen et al. Reference Hagen, Sullivan, Schmidt, Morris, Kempter and Hammerstein2009; Sorensen-Forbey et al. Reference Sorensen-Forbey, Harvey, Huffman, Provenza, Sullivan and Tasdemir2009; Sullivan et al. Reference Sullivan, Hagen and Hammerstein2008).
Second, M&S have proposed a range of new or novel adaptive behaviors associated with drug use without considering how they might negatively affect existing cognitive mechanisms. For example, M&S propose that people may use drugs for “improved social interaction” (sect. 4.2.1). Primates are characteristically “social” and can be assumed to have cognitive adaptations to facilitate sociality and attention. One must assume that natural selection has “shaped” those adaptations to perform well on average. Any drug that affects the nervous system is also going to interfere with the existing primate mechanisms for sociality. How do we, or M&S, know that this interfering with the primate nervous system is going to improve or impair the existing mechanisms for sociality? M&S seem to have given this little thought, and their account is somewhat naïve in that no reference is made to the possibility of drugs causing impairment in social cognition. After all, there is overwhelming evidence that drugs such as alcohol interfere with other cognitive mechanisms, such as those involved with motor control.
M&S reiterate this theme in their proposal that drug use increases sensory curiosity and expands perceptual horizon. Given that all mammals have evolved senses, perception, and attention to survive and reproduce in their various environments, how is interfering with these existing mechanisms an adaptation? M&S do not address the possibility of impairing existing sensory adaptations. Again, their accounts seem somewhat hopeful at best.
Third, we disagree with M&S's characterization of our notion of “the paradox of drug reward.” Our idea is that there is a conflict between the evolutionary biological view that plant toxins evolved to deter animal herbivores, and current proximate neurobiological models that argue that commonly used drugs (which are also plant toxins or their close chemical analogs) are rewarding in animal nervous systems. M&S propose that the “‘paradox of drug reward’ may be resolved at the dose-response level: In a low- to medium-dose range, the drug effect is not toxic in the sense of being an immediate threat to life. In the range of medium to low doses, therefore, a role for drugs in functional adaptation can reasonably be considered” (sect. 2, para. 2). We do not disagree with the latter part of M&S's statement, at least, but we are unclear what it has to do with the paradox. M&S seem to be saying that the “goal” of the toxin-bearing plant is to kill the herbivore, whereas functional benefits may occur at the sub-lethal dosage. Here M&S appear to have made the Spencerian “survival of the fittest” error with the presumption that evolution requires lethal selection. In reality, chemical defenses in plants are more likely to interfere with herbivore feeding and reproduction, not to kill them, and the dosage that will achieve this is different for insects and mammal herbivores in their respective ecological niches. The possible range of chemical defense dosages from wild plants indeed allows the possibility of functional benefits for invertebrates and vertebrates, as we have previously argued and outlined in great detail in the papers that M&S cite.
Finally, M&S include a section on the implications of their model for drug policy (sect. 7). In our view, M&S's ideas need development, and it is premature to make policy recommendations.