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JournalArticle 1: Marks, D. F. (2016). Dyshomeostasis, obesity, addiction and chronic stress. Health Psychology Open, 3(1), 1-20.
doi: 10.1177/2055102916636907.

Abstract: When eating control is overridden by hedonic reward, a condition of obesity dyshomeostasis occurs. Appetitive hedonic reward is a natural response to an obesogenic environment containing endemic stress and easily accessible and palatable high-energy foods and beverages. Obesity dyshomeostasis is mediated by the prefrontal cortex, amygdala and hypothalamic–pituitary–adrenal axis. The ghrelin axis provides the perfect signaling system for feeding dyshomeostasis, affect control and hedonic reward. Dyshomeostasis plays a central role in obesity causation, the addictions and chronic conditions and in persons with diverse bodies. Prevention and treatment efforts that target sources of dyshomeostasis provide ways of reducing adiposity, ameliorating the health impacts of addiction and raising the quality of life in people suffering from chronic stress.

Journal Article 2: Parent, M. B. (2016). Dorsal hippocampal-dependent episodic memory inhibits eating.Current Directions in Psychological Science, 25(6), 461-466.
doi:10.1177/0004867411432071.

Abstract: Research regarding how the brain regulates eating behavior has focused largely on homeostatic (i.e., need-based) and hedonic (i.e., pleasure-based) controls. By contrast, there is a large gap in our understanding of how brain areas involved in cognitive processes, such as memory, impact energy intake. Moreover, compared to meal size and satiety, little is known about how the brain controls meal timing and frequency. My research team and I hypothesize that dorsal hippocampal neurons, which are critical for episodic memory of personal experiences, form a memory of a meal, inhibit meal initiation during the period following that meal, and limit the amount ingested at the next meal. I review evidence supporting this hypothesis and raise the possibility that impaired dorsal hippocampal function contributes to diet-induced obesity.

Journal Article 3: Miller, G. D. (in press). Appetite regulation: Hormones, peptides, and neurotransmitters and their role in obesity.American Journal of Lifestyle Medicine.
doi: 10.1177/1559827617716376.

Abstract: Understanding body weight regulation will aid in the development of new strategies to combat obesity. This review examines energy homeostasis and food intake behaviors, specifically with regards to hormones, peptides, and neurotransmitters in the periphery and central nervous system, and their potential role in obesity. Dysfunction in feeding signals by the brain is a factor in obesity. The hypothalamic (arcuate nucleus) and brainstem (nucleus tractus solitaris) areas integrate behavioral, endocrine, and autonomic responses via afferent and efferent pathways from and to the brainstem and peripheral organs. Neurons present in the arcuate nucleus express pro-opiomelanocortin, Neuropeptide Y, and Agouti Related Peptide, with the former involved in lowering food intake, and the latter two acutely increasing feeding behaviors. Action of peripheral hormones from the gut, pancreas, adipose, and liver are also involved in energy homeostasis. Vagal afferent neurons are also important in regulating energy homeostasis. Peripheral signals respond to the level of stored and currently available fuel. By studying their actions, new agents maybe developed that disable orexigenic responses and enhance anorexigenic signals. Although there are relatively few medications currently available for obesity treatment, a number of agents are in development that work through these pathways.