Neural circuits implicated in drug conditioning, craving and relapse overlap extensively with those involved in natural reward and reinforcement like food. Exposure to drug-related cues in human addicts results in drug craving and localized activation of central circuits that are known to mediate cue-induced reinstatement of drug-seeking behavior in animal models of relapse. Similar regional activation patterns occur in humans in response to cues associated with foods. Furthermore, drug- and food-related cues not only activate common neuroanatomical regions but also result in similar activity-regulated gene expression programs within these shared areas. Cues predictive of food availability are powerful modulators of appetite as well as food-seeking and ingestive behaviors. The upregulation of a number of early genes in unique patterns within corticostriatal, thalamic, and hypothalamic networks suggests that food cues are capable of powerfully altering neuronal processing in areas mediating the integration of emotion, cognition, arousal, and the regulation of energy balance. The dopaminergic, enkephalinergic, and fos gene expressions are important regulatory genetic pathways for food craving behaviors. An umbrella term to describe common genetic antecedents of multiple impulsive, compulsive and addictive behaviors is Reward Deficiency Syndrome (RDS). Individuals possessing a paucity of serotonergic and/or dopaminergic receptors and an increased rate of synaptic dopamine catabolism, due to high catabolic genotype of the COMT gene, are predisposed to self-medicating any substance or behavior that will activate dopamine release including alcohol, opiates, psychostimulants, nicotine, glucose, gambling, sex, and even excessive internet gaming, among others. Finally, utilizing the long term dopaminergic activation approach will ultimately lead to a common safe and effective modality to treat RDS behaviors including aberrant food and drug craving behaviors.

The purpose of this review is to familiarize readers with the role that addiction plays in the formation and treatment of obesity, type 2 diabetes and disorders of eating. We will outline several useful models that integrate metabolism, addiction, and human relationship adaptations to eating. A special effort will be made to demonstrate how the use of simple and straightforward nonlinear models can and are being used to improve our knowledge and treatment of patients suffering from nutritional pathology. Moving forward, the reader should be able to incorporate some of the findings in this review into their own practice, research, teaching efforts or other interests in the fields of nutrition, diabetes, and/or bariatric (weight) management.

As obesity, type 2 diabetes (T2DM) and the metabolic syndrome sweep across the research and the clinical landscape of medical care, effective pharmacologic remedies for the treatment of obesity have become imperative. The complexities of nutrient impact on neurotransmitter and endocrine modulating chemistry have become increasingly better characterized as have the basic neurochemical pathways that mediate their effects. Food addiction has emerged as an important phenomenon that may help to explain and improve our capabilities of rendering bench lab research into impactful clinical intervention. Against this challenging backdrop of current research and study we introduce the notion that food may in fact, itself, represent a type of drug. In this review chapter of food as a drug, we outline some of the emerging science that argues how proteins, carbohydrates and fats operating on three basic levels of organismic functioning may constitute the most powerful drugs we have available to effectuate weight loss or weight gain over time. In addition, certain foods may not only be more addictive than others, but may actually have a direct effect on pro-inflammatory mediators that determine both metabolic dysfunction as well as overall neuropsychiatric function and well-being.

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