<h4>Background</h4>Ultra-processed foods (UPFs) account for approximately 38% of the adult diet, corresponding with a global increase in the prevalence of mental illnesses. Understanding the relationship between UPF consumption and mental health is crucial for public health and clinical practice.<h4>Objectives</h4>To uncover the association between consumption of ultra-processed food (UPF), dysregulated lipid metabolism, and increased risk of mental illnesses, including depression, anxiety, attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), eating disorders (ED), and food addiction (FA). In addition, this review explores the potential biological and behavioral mechanisms that may underlie these associations for each disorder.<h4>Methods</h4>Following the PRISMA extension for scoping reviews guideline, a comprehensive search was conducted across PubMed, Web of Science, and EMBASE databases. The retrieved records, screened using Covidence, included English-language studies published between 2020 and 2025 that involved participants without significant comorbidities. Relevant data on associations and proposed mechanisms were extracted and synthesized using a narrative approach.<h4>Results</h4>UPF consumption was associated with dysregulated lipid metabolism and increased risk of Anxiety, Depression, ADHD, Autism, ED, and FA. Dose-dependent increases in risk were identified in all mental illnesses except for autism. Proposed mechanisms for all these increased risks included systemic low-grade inflammation, alterations in neuronal signaling, particularly dopamine and serotonin signaling pathways, and the influence of UPF additives on neurochemical regulation.<h4>Conclusion</h4>There is a strong association between UPF consumption, disrupted lipid metabolism and increased risk of mental disorder in populations without significant comorbidities. Diets rich in minimally processed foods appear protective. The findings support the potential of pub Studies were included if they compared the effect of high and low levels of UPF consumption with the risk of developing a psychiatric disorder, or if they investigated the mechanisms related to how UPFs may cause lipid dysregulation in the context of the pathophysiological mechanisms involved in the development of mental health disorders. Disorders included in the literature review were depression and anxiety, addiction-related disorder (food addiction), eating disorders This allows the perseverance of unhealthy habits and adherence to uniformly processed foods ( 120 ). The presence of a food addiction (FA) as a comorbid problem in the setting of an ED is generally more severe than when it occurs in the absence of a comorbid ED ( 121 ). This may in part be due to a so-called “addiction transfer,” which may occur as a potential coping mechanism in mental illness ( 91 ). In fact, FA and BED may, in some cases, co-occur ( 121 , 122 ). BED, bulimia nervosa (BN) and anorexia binge-purge type have also been found to be associated with a condition known as Loss of Control Binge Eating (LCBE), which has a complex etiology ( 47 ). 3.4.2. – High-carb and added-fat UPFs trigger striatal dopamine responses similar to addictive substances; carb-fat combo has synergistic effect on reward. – Altered food matrix → faster consumption, greater bioavailability → upper intestine signals dopamine → more addictive. – Additives (artificial flavors, texturisers) enhance flavor and mouthfeel. – Low-socioeconomic areas → high UPF availability → greater reliance and higher UPF addiction. – Suggests changing the “all foods fit” approach to ED recovery to exclude or significantly reduce UPFs ( 47 ) – – UPF are highly palatable due to the taste enhancer ingredients ( 130 ) – – – Great overlap between SUDs and BN/BED, including reward dysfunction, emotion dysregulation, and impulsivity – Dominance of UPF in diet similar to addiction epidemic leading to increases in BED, obesity and cardiometabolic diseases – Suggests that education and treatment alone are insufficient to overcome UPF addiction -> need policy initiatives such as increased taxation and limitations on product availability – Emphasis on protecting youth, e.g., through restricting marketing ( 128 ) – – Additives in UPF that improve flavor and texture can stimulate dopamine, similar to substance use –> evoke food craving, and trigger binge episodes – ( 131 ) – – Dopamine downregulation – Increases in glucose and insulin levels, which can contribute to overeating UPF is associated with reward regions similar to drugs – ( 129 ) – Leptin and ghrelin levels were not significantly altered Involvement of the reward centers is proposed, visual stimuli of UPF and association with increased energy and increased intake UPF have faster transit times, meaning mechanisms to signal satiety and stomach stretching are slower, causing overeating UPF is associated with increased eating rate and increased energy intake Recommend against UPF consumption in food addiction, eating disorders ( 126 ) – UPF alter satiety and allows for overconsumption UPF consumption is significantly associated with ED and FA Dose-dependent response found – ( 123 ) – – UPF can be a form of “addiction transfer” and a coping mechanism Statistically significant correlation of UPF vs. Mechanisms linking UPF with food addiction Some of the key mechanisms in which UPF may contribute to FA include its effects on the reward system ( 47 , 121 , 128 , 129 ) ( Table 2 ). There have been previous neuroimaging-based studies that have shown similar reward patterns and loss of control deficits among individuals with FA and substance use ( 132 , 137 ). Consumption of UPF resulted in heightened levels of reward activity in the caudate and anterior cingulate regions ( 137 ). This may be mediated by the high palatability of UPF ( 137 ). The carbohydrates associated with UPF may be addictive due to their stimulation of dopamine ( 121 , 137 ).