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Stressed Out and Fed Up: The Effect of Stress on Maternal Feeding Behaviors and the Moderating Role of Executive FunctioningMendiola, Isabel 01 January 2018 (has links)
Stress is associated with a range of unhealthy eating habits. However, no previous studies have used experimental design to take an intergenerational perspective in the examination of how stress may influence parental feeding behavior, nor have they examined potential protective factors. The current study tests the effects of stress on maternal feeding behaviors and explores the potential protective role of maternal executive functioning (EF). We manipulated maternal stress with the Trier Social Stress Task (TSST) in a community sample mothers (N = 61, Mage = 33.45 years). We measured maternal EF with a series of computerized tasks. Maternal feeding behavior was observationally coded using standardized procedures. Results indicate a main effect of stress on controlling feeding styles. Furthermore, this effect of stress on controlling feeding behaviors is ameliorated among mothers with higher levels of EF. Results suggest potential factors to be considered in the treatment and prevention of diet-related illnesses.
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A Descriptive Study of Parenting Styles, Parental Feeding Behaviors and BMI Percentiles in School-age Children and AdolescentsSmith, Stephanie Jane 22 July 2008 (has links)
No description available.
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Serotonin, Norepinephrine, and the Hypothalamic Ventromedial Nucleus: a Proposed Mechanism Mediating Hyperphagia and ObesityMcDermott, Kathy Howard 05 1900 (has links)
Serotonin has been implicated as a modulator of feeding behavior. This experiment was designed to alter brain serotonin levels through dietary means in hypothalamic ventromedial-lesioned and unlesioned rats. Daily food, water, and animal weights were measured. The purpose was to determine if VMH lesions altered the feeding pattern found in unlesioned rats. Although food intake for tryptophanenriched diets and tryptophan-deficient diets did not differ from their respective control groups, in some cases gross animal weights did differ significantly between experimental and control groups and between lesioned and unlesioned groups. A proposed model explains how a "low" energy signal and a "high" protein signal cycles amino acids through gluconeogenesis to comPensate for an energy deficit.
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