Neurobiological Consequences of High-Fat High-Sugar Diets on the Mesocorticolimbic System: a Narrative Review

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dc.contributor.authorAtar, Aslihan
dc.date.accessioned2026-01-31T15:08:13Z
dc.date.available2026-01-31T15:08:13Z
dc.date.issued2026
dc.departmentİstanbul Beykent Üniversitesi
dc.description.abstractPurpose of ReviewThis narrative review aims to examine the neurobiological consequences of high-fat, high-sugar (HFHS) diets on the mesocorticolimbic reward system. Emphasis is placed on how dopamine and opioid signaling interact to drive maladaptive behaviors such as compulsive eating and food addiction.Recent FindingsHigh-fat, high-sugar (HFHS) diets have a profound impact on the mesocorticolimbic reward system, altering the function of both dopamine and opioid signaling. Evidence from animal and human studies shows that acute consumption of HFHS foods produces supra-additive effects, boosting dopamine release in the Ventral Tegmental Area-Nucleus Accumens (VTA-NAc) pathway and enhancing pleasure through mu -opioid receptor activation, which reinforces repeated intake. Chronic exposure, however, results in maladaptive neuroplasticity, including downregulation of D2 receptors, weakened dopamine signaling, synaptic desensitization, and structural impairments in the prefrontal cortex. These changes parallel neural adaptations observed in substance use disorders, manifesting as tolerance, loss of control, and cue-induced craving. The opioid system also contributes to stress-related comfort eating. In contrast, individual variability in response to treatments such as the opioid antagonist naltrexone has been linked to genetic factors, including Opioid Receptor Mu 1 (OPRM1) polymorphisms.SummaryHFHS diets profoundly reshape the brain's reward circuitry, promoting tolerance, craving, and compulsive consumption that mirror substance addiction. These findings support the conceptualization of food addiction as a neurobiological condition and highlight the importance of personalized treatment approaches. A better understanding of dopaminergic and opioid system interactions will inform targeted interventions to prevent and manage diet-related obesity and eating disorders.
dc.description.sponsorshipBeykent University
dc.description.sponsorshipOpen access funding provided by the Scientific and Technological Research Council of Turkiye (TUB & Idot;TAK).
dc.identifier.doi10.1007/s13668-026-00729-5
dc.identifier.issn2161-3311
dc.identifier.issue1
dc.identifier.pmid41543783
dc.identifier.scopus2-s2.0-105027706005
dc.identifier.scopusqualityQ1
dc.identifier.urihttps://doi.org./10.1007/s13668-026-00729-5
dc.identifier.urihttps://hdl.handle.net/20.500.12662/10628
dc.identifier.volume15
dc.identifier.wosWOS:001662330200001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringernature
dc.relation.ispartofCurrent Nutrition Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccess
dc.snmzKA_WoS_20260128
dc.subjectHigh fat high sugar diet
dc.subjectMesocorticolimbic system
dc.subjectFood addiction
dc.subjectNeuroplasticity
dc.titleNeurobiological Consequences of High-Fat High-Sugar Diets on the Mesocorticolimbic System: a Narrative Review
dc.typeReview Article

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