Association for Behavior Analysis International

The prevalence of obesity continues to climb in all age groups, and around the world. The standard paradigm assumes that we “eat too much and exercise too little, that obesity is due to two aberrant “behaviors”. However, are these behaviors cause or effect? Our research on children with brain tumors who develop hypothalamic damage and become obese after surgery or radiation, termed “hypothalamic obesity”, demonstrates that they have anatomic “leptin resistance”. In these subjects, excessive insulin release blocks leptin signaling to drive weight gain and hunger, while pharmacologic insulin suppression results in reduced food intake, increases spontaneous activity, and promotes weight loss. Why should insulin block leptin signaling? Leptin is a necessary signal to the VMH for the initiation of high-energy processes, such as puberty and pregnancy. If leptin always worked, then nobody could gain weight, and our reproductive capacity would be shot. Most obese people are hyperinsulinemic. But is that cause or effect? It is assumed that as you gain weight, cytokines are released from adipose tissue, which drive insulin resistance. However, our research demonstrates that dietary sugar is metabolized to fat in the liver, and it is this liver fat that drives insulin resistance unrelated to peripheral fat. Why should sugar drive insulin resistance? Naturally occurring sugar in fruit is what makes fruit palatable. But for our ancestors, fruit was readily available for one month per year, called “harvest time”. Then came four months of winter, and no food at all. We needed to stock up, to increase our adiposity in preparation for four months of famine. In other words, seasonal insulin resistance was evolutionarily adaptive; but year-round insulin resistance due to ubiquitous sugar availability has become maladaptive. It is assumed that people consume sugar because of its palatability. However, there is now evidence that sugar may be addictive in humans. Obese subjects will use sugar to treat psychological symptoms. Overweight women who were self-reported carbohydrate cravers reported greater relief from dysphoria in response to a carbohydrate-containing beverage as compared to a protein drink. Why are we drawn to sweet? Evolutionarily, sweetness was the signal to our ancestors that a given food was safe to eat because there are no sweet foods that are acutely poisonous (even Jamaican vomiting sickness only occurs after consumption of unripe ackee fruit, which is not sweet). Unfortunately, the food industry knows this and adds excess sugar to processed food to make us buy more. Thus, the behaviors associated with obesity are secondary to our biochemistry, and our biochemistry is secondary to our environment. Understanding these evolutionary precepts explain our obesity epidemic, and also point to environmental and policy solutions.

Practitioners working in behavioral medicine settings or environments where dietary issues impact behavioral responses.

B. F. Skinner argued that neurobiology was not necessary to explain operant behavior. However, some of his most publicized conjectures could only be tested using neurobiological methods. For instance, 1959, in what may be one of the most decisive debates in modern psychology (or cognitive neuroscience), Noam Chomsky gutted Skinner's claims that human language were acquired via operant processes. By understanding and comparing the neurobiological mechanisms of operant learning in different animals, we now are beginning to accumulate evidence that Skinner was at least partially correct: there is a dedicated, evolutionarily conserved biochemical mechanism underlying behavioral learning which does not seem to be involved in the other forms of learning tested so far. This mechanism is also involved in acquiring at least the speech component of language, articulation. Coincidentally, such experiments also solved a technical problem first formulated by Skinner in 1935. Behavioral experiments were performed ~80% statistical power and have been internally replicated before publication. These replications often included different genetic modifications targeting the same biological structure, providing converging evidence for any given effect.

Fellow researchers, but it is my aim that graduate students should be able to follow and understand the talk nevertheless.

Methods to support students' competencies often target isolated contexts or activate individual treatment agents. Conjoint Behavioral Consultation (CBC; Sheridan, Kratochwill & Bergan, 1996; Sheridan & Kratochwill, 2008), on the other hand, is an indirect intervention focused on the attainment of students' goals through (a) collaborative and consistent implementation of evidence-based interventions across home and school settings, and (b) data-based problem solving with parents and teachers working as partners. This presentation will review CBC and decades of empirical investigations that have documented its efficacy for promoting behavioral, social-emotional and academic competencies among children facing a range of behavioral and learning challenges. Research exploring outcomes for students, parents and teachers will be presented. A focus on translation and considerations for practice will be highlighted by exploring empirically-derived "active ingredients" (mediators) responsible for CBC's effects, conditions (moderators) under which desired outcomes are maximized, and a number of implementation lessons learned. Opportunities for future research and training will be explored.

Professionals who serve as consultants or who are interested in school/home consultation.