Binge-eating disorder (BED) as defined by compulsive overeating during recurrent “eating attacks” constitutes the most common eating disorder in the Western world. Despite being associated with serious metabolic and psychiatric co-morbidities, we only have a limited understanding of its etiology, and particularly, the mechanisms defining inter-individual risk. Here, we identify a Tet1-dependent epigenetic mechanism that is instrumental in setting inter-individual BED susceptibility thresholds via tuning the midbrain dopamine (mDA) reward neurocircuitry. By intersecting in-vivo fiber photometry and chemogenetics, we find that maladaptive hyperactivation of mDA neurons is necessary for driving experimental BED (eBED) in mice: a feature distinguishing it from conventional obesity mouse models. Nuclear sorting and DNA methylome analysis reveal that eBED triggers rapid and highly specific increases in 5-hydroxymethylcytosine (5hmC) marks in mDA neurons over genes known to regulate addictive behaviors in response to drugs of abuse (e.g., cocaine). These data suggested a potential role for DNA hydroxymethylation in addiction-like eBED responses to food. Intriguingly, the de-/hydroxymethylation enzyme TET1 is highly enriched in mDA neurons, and heterozygous loss of Tet1 in either a global or in an mDA-specific manner increased variability in eBED vulnerability across isogenic littermates, with phenotypes ranging from wild-type-like susceptibility to complete resistance. Comparing eBED prone versus resistant animals revealed pronounced changes in the input-output architecture of the mesocorticolimbic mDA neurocircuitry. Specifically, we found that eBED prone mice exhibited significantly increased bidirectional connectivity between the medial prefrontal cortex and the VTA as characterized by an elevated dopaminergic tone and higher numbers of layer 5 pyramidal (L5pyr) neurons. Intriguingly, selectively inhibiting this VTA-projecting subset of L5pyr neurons via chemogenetics was able to prevent the development of voracious binge-eating. Thus, Tet1 dosage determines individual food reward thresholds and provides empirical evidence suggesting that a substantial fraction of addictive vulnerability is epigenetically defined.