Based on current knowledge, it can be assumed that most of the changes in appetite-regulating peripheral peptide hormones, neuropeptides, and neurotransmitters described in eating disorders correspond to secondary physiological adaptation processes to altered food intake (state markers). Depending on the type of eating disorder (e.g., anorexia nervosa versus bulimia nervosa), the changes are partly expressed in opposite directions. However, more and more studies indicate that central and peripheral effects of altered energy intake may contribute to the maintenance of pathological eating behavior. Recent publications have not been able to confirm the results of earlier studies in some cases. Instead, it has been shown that for some mediators, the measured results also strongly depend on the pre-analytics (especially for unstable mediators) or the respective analysis methods. Furthermore, it is becoming increasingly clear that differences may also be due to the respective composition of the patient cohort and their specific clinical characteristics. If standardized meals are part of the study design, the nutrient composition and possibly the hedonic value (pleasure in eating very tasty dishes instead of meeting energy requirements) seem to play a role. Last but not least, for neuroendocrinology, many previous studies were based on too small sample sizes, which can make replication more difficult.