In response to stress, stress-sensitive systems, including the sympathetic-adrenal-medullary (SAM) axis and the hypothalamic-pituitary-adrenal (HPA) axis, are activated to enable the individual to engage in the fight-or-flight response resulting in catecholamine (e.g., epinephrine and norepinephrine) and cortisol release. Stress-induced cortisol secretion has been shown to elicit a decrease, increase, or no change in the homeostatic mechanisms of food intake (e.g., appetite, appetite hormones, food intake). However, homeostatic control can be overridden by hedonic (or pleasure-inducing) mechanisms. Stress can increase cravings of unhealthy palatable food causing alterations in food preference (e.g., sweet foods), enhancing the motivation for their acquisition (i.e., food reward). Mapping the evidence and identifying gaps of acute psychological stress on food intake regulation serves as the purpose of this scoping review. Methods: Four databases (PubMed, Medline, Web of Science, PsycInfo) and grey literature were searched using predetermined keywords. Participant characteristics, types of stressor used, food intake mechanism assessed, and the primary findings were extracted. Results: Of 9953 abstracts, 37 articles were included for data extraction. Stress increased food cravings and liking for palatable foods and heightened the food reward response, while some studies expressed no change. Studies favoured the measurement of homeostatic mechanisms (primarily food intake), suggesting the need for non-homeostatic measurements, particularly food reward. Conclusions: Overlap between homeostatic and non-homeostatic mechanisms (e.g., subject’s inability to dissociate between homeostatic hunger and hedonic hunger), types of psychological stressors used, study design (e.g. time course of assessing outcome measures post-stressor), and the influence of moderating variables (e.g., cortisol reactivity, emotional eating, body mass, chronic stress, dietary restraint) aid in the explanation of incongruous results pertaining to acute psychological stress and food intake. In addition to establishing standardized protocols for assessing the effects of acute psychological stress on food intake regulation, three areas of focus for future research should be placed on: (1) increasing appetite hormone assessment (e.g., GLP-1, leptin, ghrelin), (2) developing appropriate definitions/theories for non-homeostatic mechanism assessment (e.g., distinguishing food reward from food craving), and (3) expanding the research population to explore how sex, age, and body mass status may influence food intake regulation in response to acute stress.