I don't really think that real food is necessarily hijacking anything. It all appears to depend upon leptin sensivity, which likely predisposes us to becoming slaves to food addiction in the first place.
Leptin resistance: a prediposing factor for diet-induced obesity
This review examined several models of leptin resistance and the role of leptin resistance in the susceptibility to dietary obesity. Only some of the leptin-resistance models (leptin antagonist blockade and aged obese rats) exhibit heightened weight and adiposity gain on a chow diet, while all models discussed demonstrate obesity in the presence of an HF diet. Thus, the leptin resistance appears to be reinforcing “reward eating” beyond caloric energy requirements. Overconsumption of palatable food could be mediated by activation of reward circuitry involving opioids and dopamine or an impairment in a pathway (or pathways) mediating satiation of the palatable diet (16).
Whereas the hypothalamus, in particular, the arcuate nucleus, has been identified as important in regulating the caloric requirements, other regions in the hypothalamus, such as lateral hypothalamus and extrahypothalamus areas including the amygdale, prefrontal cortex, nuclear accumbens, and ventral tegmental area (VTA), are implicated in the reward properties of food (12, 43). Leptin receptors are identified on dopamine-containing neurons within the VTA and were found to suppress dopaminergic neuron firing rate (24). They act through the JAK-STAT signaling pathway and decrease food consumption upon leptin action. The fact that a chronic reduction in leptin receptor activity in the VTA by siRNA knockdown enhances sensitivity to highly palatable food underscores an important role of leptin receptor function in the regulation of reward feeding behavior (24). Our own data also support a counterregulatory mechanism by which leptin modulates HF feeding: leptin receptor blockade prolonged the caloric hyperphagia induced by an HF diet (67). Although, the inputs from multiple brain regions are integrated to determine food ingestion, hedonic feeding driven by the VTA has been suggested to be able to overcome the caloric requirements of homeostatic regulatory properties of the hypothalamus (12).
And that is my best guess as to why I don't overeat even when the real food is ridiculously yummy, because I'm full and satisfied since the real food hasn't pwnt my lectin receptor sensitivity. Food reward is there to make us eat in the first place, and it isn't the body's design to harm itself needlessly, unless it is already harmed.