Researchers from Spain’s National Center for Cardiovascular Investigation have identified a surprising ally in newborn heart health: gamma-linolenic acid found in breast milk. In mice, this fatty acid helps keep a baby’s heart function steady after birth by supporting the energy systems that drive the heart. The findings point to new avenues for treating mitochondrial disorders and were detailed in a major scientific journal.
When a mammal is born, its heart must switch from relying on the placenta to generating energy on its own. To do that, heart muscle cells must kick their mitochondria into gear, producing the energy needed to keep the heartbeat steady. Until now, scientists had limited insight into the signals that prompt this crucial metabolic transition right after birth.
What the team discovered is that gamma-linolenic acid in breast milk binds to a protein called RXR inside heart cells. This interaction turns on a set of genes that supply mitochondria with the proteins necessary to burn fat, which becomes the main energy source for a mature heart. In other words, a natural component of breast milk acts as a signal and a fuel selector, guiding the newborn heart to switch on its fat-burning machinery exactly when it is needed.
Experiments in mice showed that removing RXR from heart cells, or lacking gamma-linolenic acid in the milk, prevents the heart’s mitochondria from producing enough energy in the first days after birth. The consequence is a rapid decline in heart function and, in some cases, fatal heart failure within about two days after birth. The results underscore how tightly new-born heart metabolism is tied to the nutritional and signaling environment provided by maternal milk.
Experts explain that birth is a major physiological ordeal for newborns. Beyond nutrition, breast milk appears to carry signals that tell cardiomyocytes to shift their energy metabolism as maternal support ends. This signaling role complements the well-known nutritional benefits, highlighting a dual function of breast milk in early life nutrition and developmental guidance for the heart.
The work opens possibilities for treating mitochondrial diseases by modulating RXR activity in heart cells with targeted drugs. By adjusting this signaling axis, it may be possible to support or restore proper energy production in dysfunctional hearts, offering a potential new strategy for conditions rooted in mitochondrial failure. The researchers emphasize that further studies are needed to translate these findings into safe, effective therapies for human patients, but the concept lays a foundation for future clinical exploration. The discovery adds a compelling layer to our understanding of how breast milk supports infant development beyond basic nourishment, tying maternal biology to the neonatal heart’s energy needs and resilience. The insights align with a broader interest in signaling mechanisms that govern organ maturation after birth and how these processes can be harnessed for medical advances.