Seven percent of New Zealand’s babies are born prematurely. As these children grow up, even those who were considered healthy at the time of discharge face an increased risk of cardiovascular disease in adulthood. Omega-3 is essential for normal cardiovascular tissue development. In the foetus, omega-3 is maintained at high levels whereas following premature birth, levels fall dramatically. This decrease persists, such that by term equivalent age, infants born preterm have significantly lower omega-3 than those born at term. This ‘preterm deficit’ may explain some of the later preterm-associated cardiovascular dysfunction, and its correction may offer novel therapeutic opportunities to prevent long-term cardiovascular morbidity. In humans, the latency between birth and adult-onset disease limits the speed with which new therapeutic opportunities can be fully explored. By using our established small animal model, this latency is reduced, enabling timely data acquisition, knowledge dissemination, and ultimately, better outcomes for those affected by preterm birth.