Association for Behavior Analysis International

Subject-rated measures and drug self-administration represent two of the most commonly used methods of assessing the behavioral effects of drugs in the human laboratory. Although the results from these methods are often consistent, dissociations between subjective and self-administration data have been observed. This presentation will first introduce basic human behavioral pharmacology methods for measuring subjective and reinforcing effects of drugs, focusing on representative data from commonly abused stimulants. Second, correlational and regression analyses that examined the relationships between subjective and reinforcing drug effects will be presented to demonstrate which subjective measures best predict stimulant self-administration. Third, examples of divergence between subjective and reinforcing drug effects will be explored to show how these measures provide different and complementary information about stimulant drug effects. Potential mechanisms underlying this divergence also will be considered. Finally, the implications of these outcomes as they relate to future human laboratory research and intervention development for managing drug-use disorders will be reviewed.

Psychologists, behavior analysts, graduate students, and anyone interested in methods of assessing the behavioral effects of drugs in the human laboratory.

The public’s attitude toward the principles and practice of behavior analysis tends to range from complete unawareness to misguided hostility. The result is that the field is often marginalized, even as it becomes potentially ever more valuable as a means of addressing difficult, widespread problems in society in important behavior-related domains, including education, population, health, economics, and climate change. The public’s ignorance, misperceptions, and apprehensions about behavior analysis stem in part to a long history of prominent antagonism toward the field on the parts of those invested in alternative and generally less effective approaches to dealing with behavior. But the problem also has been exacerbated by a sharp failure on the part of the field, dating back to B. F. Skinner himself, to present itself in ways likely to resonate with the public. Meanwhile, leaders in what might be considered “rival” fields have often been, and continue to be, highly effective in doing so, sometimes to behavior analysis’s detriment. Ironically, behavior analysis’s fidelity to the rigors of scientific evidence has worked against the field in this regard. This rigor has produced effective treatments, but leaves lay people cold when it comes to understanding and appreciating this effectiveness, given that most of the public has little feel or empathy for scientific rigor, and is instead easily swayed by emotional and narrative appeal. The challenge that therefore lies before the field is this: Can and should behavior analysis present itself to an often gullible and easily misled public in a more resonant, less scientifically stiff way that wins it more appreciation and thus opportunity to achieve impact? It almost certainly could, and it’s worth considering possible approaches for doing so, as well as weighing the potential costs.

Psychologists, behavior analysts, graduate students, and anyone interested in learning about the perception of behavior analysis.

The Polyvagal Theory describes the role physiological state has in facilitating the expression of different classes of behavior. Applying the theory to behavior modification protocols leads to a refinement in the historical S-O-R model in which the state of the organism (O), now indexed by autonomic state, influences the accessibility of classes of behavior to stimulus control. Polyvagal Theory, based on evolutionary biology and comparative neurophysiology, identifies autonomic states that facilitate or impede the expression of specific classes of behavior. The theory identifies three stages of phylogenetic development that are characterized by parallel changes in behavioral repertoire and neural regulation of the autonomic nervous system: 1) an ancient autonomic system (i.e., unmyelinated "vagal" pathways) shared with most vertebrates that conserves metabolic resources (e.g., slows heart rate and breathing, decreases blood pressure) and supports immobilization behaviors (e.g., passive avoidance, fainting); 2) a system that increases metabolic output (i.e., sympathetic nervous system) and supports mobilization of the trunk and limbs (e.g., active avoidance, fight-flight behaviors); and 3) a uniquely mammalian system integrating the regulation of striated muscles of the face and head with the heart (i.e., myelinated "vagal" pathways) to create a functional social engagement system that regulates the phylogenetically older systems, often through social interaction, to promote physiological resilience and optimize health growth and restoration. Functionally, the theory proposes that modification of these "classes" of behaviors (immobilization, mobilization, and social engagement) will be optimized by monitoring autonomic variables and understanding the contextual cues that trigger transitions in autonomic state. Consistent with this model several variables, independent of stimulus manipulations, characterizing experimental conditions, and participants in behavior modification protocols (e.g., context, development, illness, medication, etc.) will influence the accessibility of different classes of behavior to stimulus control.

Graduate students, practitioners, academics, and scientists.

Adolescence is a conserved developmental period characterized by ontogenetic alterations in brain and behavior that often bear notable similarities across species, including increases in peer-directed social behaviors, risk-taking, as well as elevated per occasion use of alcohol. Studies using a rodent model of adolescence have shown that, seemingly due in part to age differences in brain function and in expression of acute tolerance, adolescents are more resistant than are adults to alcohol effects that normally serve as cues to moderate drinking, while conversely showing greater sensitivity to ethanol-induced social stimulation. To the extent that these findings in laboratory animals are relevant to human adolescents, this developmental blending of enhanced/attenuated ethanol sensitivities may encourage relatively high levels of consumption, particularly among adolescents who are otherwise at risk for especially elevated alcohol intake because of genetic or environmentally associated alterations in ethanol sensitivities Such elevated ethanol exposures may lead to adverse consequences among at-risk adolescents that may persist into adulthood. Indeed, our findings to date have revealed certain long-lasting consequences of repeated exposure to ethanol during adolescence that are replicable, specific, and dependent on timing of the ethanol exposure, with early adolescence being perhaps an especially vulnerable period, and comparable exposures in adulthood generally not inducing similar effects.

One solution that has been proposed to combat the ongoing obesity epidemic has been to replace caloric sugars with artificial sweeteners that provide sweet tastes without providing the associated calories. While such an idea seems to be common sense, scientific data supporting artificial sweeteners as beneficial for weight loss are weak. Further, more recent epidemiological data from long-term studies in a variety of human cohorts have indicated that daily consumption of artificial sweeteners may exacerbate metabolic disturbances like Type 2 diabetes, metabolic syndrome, and stroke. One explanation for such a counterintuitive result is that consuming sweet tastes without typical post-ingestive outcomes could interfere with basic learning processes that normally operate to regulate energy balance. Using data from an animal model, work from Dr. Swithers' lab has explored how interfering with predictive relations between tastes and calories may contribute to negative health outcomes. The results suggest that obesity and its attendant co-morbidities are unlikely to be helped by consuming "diet" foods manufactured with sugar substitutes.