Chronic stress has long-term adverse consequences on eating behaviour and can enhance the development of obesity. While specific brain circuits controlling stress development and feeding behaviour have been identified, how they interact is unknown. Here we uncovered that Npy-expressing neurons in the medial nuclei of the central amygdala (CeAM) provide a dual inhibitory control to both, Npy1r-expressing glutamatergic neurons in the lateral habenula (LHb) and lateral hypothalamus (LH), to promotes hedonic feeding and overrides the normal homeostatic regulation of positive energy balance. Under combined stress and HFD feeding condition (HFDS), translatome analysis of Npy-neurons from the CeAM reveals a significant increase of a unique set of active translating mRNAs controlling NPY overproduction, GABAergic neuron physiology and trans-synaptic signalling when compared to HFD-only conditions that activate predominately genes that involve lipid cellular metabolic processes. Consistent with our circuit tracing study, the loss of function deletion of Npy1r in the LHb shows a robust anti-obesifying effect due to reduced food intake under HFD conditions. Circuit tracing studies also identified a critical neurocircuit projection from the LHb-Npy1r neurons to the VTA which when opto-genetically being activated reduces feeding behaviour as well as promotes anxiety-like related behaviours. Together, these results identify CeAM-Npy neurons as a key regulatory node that controls chronic stress responses by driving palatable food intake in an attempt to overcome the negative valance of stress.