The worldwide manifest increase in the number of people with obesity challenges the public health care system. The more because obesity is increasingly observed in young people and this phenomenon enhances the time of exposure to excess adiposity with increased risk of comorbidities and secondary effects on other systems like the skeleton. Obesity is a multifactorial condition, but there is increasing observational evidence that the changed dietary pattern from traditional staple foods to ultra-processed foods (UPF) contributes to obesity. UPF are industrial formulations manufactured by deconstructing foods into their component parts, modifying them and recombining them with cosmetic additives. Still, the number of prospective cohort studies is limited, but the results of several ongoing studies are awaited. Various physiological pathways are proposed to explain how ultra-processed dietary patterns promote adiposity. First, UPF tend to have high energy density and soft texture, which increase energy consumed to satiation and promote a weaker satiety response. In addition, food processing often removes natural structural barriers to macro-nutrient digestion, thereby increasing the metabolizable energy of foods and altering nutrient absorption kinetics. These aspects might impair the release of appetite suppressing hormones like PYY and GLP1. Furthermore, these diets often contain hyperpalatable nutrient combinations (e.g >20% of calories from fat combined with >20% calories from sugar; or carbohydrates/fat and sodium). The consumption of this hyperpalatable food stimulates the food reward system more compared to the reward elicited by the single nutrient and thus increases energy intake. Additional pathways are suggested, but strong evidence is still lacking. They include disruption of gut-brain signaling of food value, modified gut microbiota and disturbed host-microbiota interactions. Taken together, excessive energy intake due to increased energy intake rate and enhanced food reward are probably the main mechanisms through which UPF promote excess adiposity. A better understanding of how UPF contribute to obesity might lead to strategies to reduce UPF consumption and create health-promoting food systems that will help to halt the rise in obesity, but policy efforts are likely needed.