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phase when they should typically be sleeping/fasting. The Clock mutant mice also consumed 22% more of their daily food intake at abnormal times (light phase) when compared to the food intake of the wild-type mice. Over the 10-week observation period, the Clock mutant mice consumed more food, had significant weight gain, and had higher levels of triglycerides, cholesterol, glucose and leptin (Turek et al., 2005). Animal literature supports the idea that timing of food intake can reinforce a phase advance or phase delay of circadian rhythm. For instance, when researchers restrict food from rodents when they typically eat at night, and only present food during the daytime hours, food anticipatory activity begins to occur at the new feeding times (Mistlberger, 2009). The circadian rhythm of the rodents becomes re-entrained to this new feeding time even though it is outside of their typical cycle. Not only does behavior shift, but biological markers of circadian rhythm do as well (e.g., insulin, glucose, leptin, ghrelin, and thyroid stimulating hormone (TSH)) (Silver and Balsam, 2010). The animal literature provides a useful model for conceptualizing the development and maintenance of dysregulated of circadian rhythm in persons with NES. Specifically, it supports the hypothesis that there are both genetic and environmental factors that can re-entrain eating behavior to abnormal times during the 24-hour sleep/wake cycle. Consistent with the animal literature, several human studies support the hypothesis that NES results from a circadian disruption. These are reviewed below. 12PDF Image | BRIGHT LIGHT THERAPY FOR late NIGHT EATING SYNDRome
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