Binge eating is characterized as the unrestrained consumption of large amounts of food within a brief time period and is a heritable trait of eating disorders often associated with anxiety and depression. Not surprisingly, such eating disorders as Bulimia Nervosa (BN) and Binge Eating Disorder (BED), associate strongly with heightened impulsivity and drug seeking behavior. Due to these conditions being heritable, this suggests there is a common genetic basis driving these behaviors. However, the genetics behind restraint when faced with palatable food and the brain nuclei that may be activated still remains unclear. We report here that different genetic mechanisms likely drive ad libitum food intake when compared to binge feeding behavior. Through studying the food intake patterns of female mice from four Diversity Outcross (DO) founder inbred strains (C57Bl/6J (B6), NOD/LtJ (NOD), 129S1/SvlmJ (S1), and A/J (AJ)), we discovered no differences among three of the strains during ad libitum feeding of both chow and high calorie diet (HCD), while the AJ strain showed elevation with both. Interestingly, when a separate group of mice underwent induced binge feeding, we discovered significant variation among the strains during the 3hr and 24hr binge feeding periods. In addition, we were able to define specific brain nuclei that showed differences in neuron activation between the inbred strains that may be responsible for driving the observed differences in binge feeding behavior. Future studies could use these brain areas in order to potentially discover the variations across the genome that modulate binge eating behavior.