Ageing is a conserved feature of metazoan life whose rate is profoundly sensitive to dietary intake. While specific nutrient-sensing mechanisms allocate physiological resources to growth, reproduction, and somatic maintenance, the precise ways in which combinations of dietary components engage these programs to influence ageing and survival remain poorly understood(1). This study aimed to dissect these interactive networks by examining how combined essential nutrient deprivations affect life history traits. Adult female fruit flies (Drosophila melanogaster) were subjected to a fully factorial experimental design utilizing 16 dietary conditions (n=100 per condition). These diets comprised a fully fed (FF) control and all possible single, pairwise, three-way, and four-way deprivations of phenylalanine (Phe), methionine (Met), cholesterol (Cho), and zinc (Zn). To evaluate the variability and significance of the results, lifespan data were analysed using a mixed-effects Cox proportional hazards model and log-hazard ratios (log-HR), while egg production dynamics were assessed via a linear mixed-effects model and a non-linear mixed-effects exponential decay model. Survival analysis revealed that all main and interactive effects of nutrient deprivation significantly altered lifespan (four-way interaction χ² = 38.5, p < 0.001). Individually, Met or Cho deprivation severely reduced median lifespan compared to the FF control (Met: 26.0 days, Cho: 29.9 days, FF: 58.0 days; both p < 0.001). Conversely, Phe deprivation was phenotypically neutral regarding lifespan (60.9 days, p = 0.500), and Zn deprivation modestly extended it (65.0 days, p = 0.011). Notably, diet significantly modified egg production dynamics (Diet × Time F60,1376 = 61.4, p < 0.001), with Phe omission causing a rapid collapse (half-life 0.37 days) compared to the FF control (3.81 days). Assessment of complex interactions via log-HR classified the multi-nutrient diets into additive, negatively dominant, and antagonistic effects. Strikingly, seven diet combinations demonstrated antagonistic interactions, wherein the removal of one essential nutrient rescued the deleterious effects of another. Most notably, Phe deprivation provided broad protection, fully or partially rescuing the lethal cost of Met and Cho deficiencies (extending lifespan by up to 30 days). Meanwhile, Zn omission operated through an independent mechanism to block the detrimental effects of Cho deprivation, but not Met deprivation. Collectively, these non-additive, antagonistic effects demonstrate that essential nutrients do not merely act as passive building blocks. Instead, precise dietary manipulations reveal specific nutrient-sensing programs capable of gating whole-organism survival, indicating that amino acid-specific pathways can be leveraged to antagonise the physiological detriments of other nutrient deficits and sustain life.