While specific neurocircuits control either stress responses or feeding behaviour, the underlying neurobiology that motivates stress-eating remains unknown. In addition, the intersection of stress-responding and appetite-regulating neural pathways and the downstream neurocircuits in which they modulate are also unknown. To identify the neural populations involved in stress overriding homeostatic energy control as observed in stress-eating phenotypes, we’ve employed a systematic, non-biased approach utilising the well-established and reliable early gene marker cfos. as an indicator of neuronal activation in response to a high fat diet combined with a chronic stress paradigm. This identified the lateral habenular (LHb) as a key centre responsive to HFD and stress. Neuropeptide Y (NPY) neurons in the central amygdala were recently discovered to influence stress-eating phenotypes most likely via interacting with the anti-reward region the lateral habenula. Activation of lateral habenula neuronal populations has been shown to suppress the consumption of palatable substances, hence inhibiting the lateral habenula through the action of NPY may suppress stress-eating behaviours. Extracting actively translating mRNA from stimulated lateral habenula neurons from animals fed a high-fat diet revealed robust expression of Y1-receptors. Interestingly, animals exposed to a high-fat diet paired with a stress paradigm, the expression of these Y1-receptors was significantly attenuated. Importantly, inhibiting Y1-expressing neurons in the lateral habenula with chemogenetic technology increased palatable food consumption, which is consistent with the specific ablation of Y1 receptors studies that also prevented stress-induced obesity development. Employing viral tracing strategies unveiled that these lateral habenular Y1 receptor neurons project to reward-regulatory regions such as the ventral tegmental area and the dorsal raphe nucleus. Together these results suggest that NPY originating from the CeA influences reward regulatory regions by inhibiting lateral habenula Y1-receptor neuronal circuitries, thereby contributing to stress-eating. Targeting this neurocircuits may allow for better weight management specifically under chronic stress conditions.