Rada, Avena & Hoebel (2005): In rats with
intermittent access to sucrose, daily bingeing
repeatedly increases dopamine (DA) in the nucleus accumbens shell — a brain area central to reward and addiction.
PubMed+1
Sucrose sham-feeding study: Even when stomach content is “sham fed” (i.e., not actually digested), just tasting sugar on a binge-schedule triggers accumbens dopamine release.
PubMed
Kir2.1 Study (2017): Mice that had prolonged sucrose access, upon withdrawal, displayed
depression- and anxiety-like behaviors. At the molecular level, there was an
increase in the Kir2.1 potassium channel in the nucleus accumbens, and reduced dopamine/CREB activity.
PubMed
Neuroimmune Effects (2024): Sex-specific effects in mice — after sucrose withdrawal, male mice showed
neuroinflammatory marker increases in reward regions (PFC, NAc) and anxiety-like behavior.
PubMed
Anxiety after deprivation (2008): Rats bingeing on sucrose then fasted showed anxiety and changes in extracellular acetylcholine and dopamine in the nucleus accumbens.
PubMed
Deprivation-Effect Paradigm: Rats with intermittent sugar access show
increased sugar-seeking behavior after abstinence, similar to “craving” in drug models.
PubMed
Review of Sugar Addiction (Avena, Rada, Hoebel): A comprehensive animal model showing “bingeing,” “withdrawal,” “craving,” and “cross-sensitization” with drugs of abuse.
PubMed
Added Sugar & Placental DNA Methylation (2021): Higher maternal added sugar intake was associated with
altered DNA methylation in the placenta, as well as fetal behavior (reduced third-trimester movement) and shorter gestation.
PubMed
Review of Sugar Use in Pregnancy: A review summarizing evidence that maternal sugar intake may contribute to gestational diabetes, preeclampsia, and may affect offspring metabolism, taste preference, and obesity risk.
PubMe
DTI Study in Infants (2021): In human infants,
higher prenatal maternal sugar intake (particularly “added sugar”) was associated with differences in brain tissue organization (via diffusion tensor imaging). The authors suggest this may reflect altered dendrite/synapse formation in gray matter.
MDPI
Project Viva – Cognition Study (2018): In a cohort of ~1,234 mother-child dyads,
higher maternal sucrose intake and sugar-sweetened beverage consumption during pregnancy was linked to
lower cognitive scores in mid-childhood (non-verbal IQ), after adjusting for confounders.
PubMed
High-Sugar Maternal Diet in Rats (2021): Maternal high-sugar intake during pregnancy/lactation impaired offspring memory, with molecular changes in NMDA receptor subunit composition in hippocampus and prefrontal cortex.
PubMed
Prenatal Sucrose in Rats (Aged Offspring, 2017): High prenatal sucrose led to worse spatial memory in aged offspring and signs of oxidative stress + altered NMDA/Wnt signaling in hippocampus.
PubMed
Epigenetic Mechanisms (Mice, 2024): A high-fat, high-sugar maternal diet in mice led to changes in offspring brain DNA-methylation enzymes (DNMT, TET) in a sex-specific way, suggesting a mechanistic pathway for neurodevelopmental risk.
PubMed
Transgenerational Cognitive Deficits (Mice): Maternal over-nutrition (high fat + sugar) in mice caused cognitive deficits not only in the immediate offspring, but across multiple generations, with changes in neurotransmitter systems.
PMC+1