The commentary was prompted in part by a recent study examining the Special Supplemental Nutrition Program for Women, Infants, and Children, the United States federal nutrition program better known as WIC. Researchers led by Yuelong Shi and colleagues found that participation in the program was associated with a reduced risk of cerebral palsy, adding to earlier findings that WIC participation is linked to fewer preterm births and lower infant mortality. For the Madrid-based neonatologists, these findings point to a broader biological story: nutritional adequacy during pregnancy is not merely a matter of birth weight or growth, but of brain integrity.

Cerebral palsy has challenged clinicians since it was first described by the British surgeon William Little in 1861. The condition arises from injury to the developing fetal or infant brain and persists throughout life, producing a heterogeneous array of motor impairments that have made it notoriously difficult to define. Modern neuroimaging has clarified much of the underlying pathology. The most common form of white matter damage visible on magnetic resonance imaging affects the periventricular region, the tissue surrounding the brain’s fluid-filled ventricles, where it manifests either as leukomalacia—a softening and death of white matter—or as hemorrhage. Injury to the deep gray matter structures, the basal ganglia and thalamus, follows as the second most frequent pattern.

These anatomical signatures are not random. The periventricular white matter is among the most vulnerable tissue in the preterm and near-term brain because it is richly populated by developing oligodendrocytes, the cells responsible for wrapping nerve fibers in myelin. When the fetal brain is deprived of oxygen, nutrients or both, these fragile cells fail or die, disrupting the wiring that coordinates movement. The commentary’s central premise is that maternal nutrition shapes how well the fetal brain withstands these insults, and that specific dietary components may confer genuine neuroprotection rather than simply supporting general growth.

Among those components, the long-chain polyunsaturated fatty acids occupy a special place. Docosahexaenoic acid, or DHA, an omega-3 fatty acid abundant in oily fish and algal oils, is a structural building block of neuronal membranes and accumulates rapidly in the fetal brain during the third trimester of pregnancy. Its omega-6 counterpart, arachidonic acid, is equally concentrated in neural tissue and plays a critical role in membrane fluidity, signaling and inflammatory regulation. Because the fetus depends entirely on placental transfer for these fats, the mother’s dietary intake and her own body stores directly determine how much of these building blocks reach the developing brain.

Experimental evidence supports the idea that this supply line matters for resilience. In a widely cited rat model of perinatal cerebral hypoxia-ischemia, researchers led by Debora Berman showed that pretreatment with DHA conferred measurable neuroprotection, reducing the brain injury that followed oxygen deprivation. The finding suggests a mechanism: a brain adequately supplied with DHA enters a hypoxic or inflammatory crisis better buffered against damage than one that is deficient. The commentary’s authors argue that this kind of mechanistic evidence, combined with the epidemiological signals from nutrition programs, justifies treating maternal LCPUFA intake as a target for cerebral palsy prevention rather than an afterthought.

The timing of fatty acid supply has become a central concern in neonatal nutrition research. A 2026 review by Simon Dyall and colleagues in Progress in Lipid Research highlighted what the field now calls the Preterm PUFA Gap: babies born prematurely are cut off from the placental transfer of DHA and arachidonic acid weeks or months before their brains would normally accumulate these fats, and standard enteral nutrition has historically failed to close the deficit. The result is an imbalance between omega-3 and omega-6 fatty acids during precisely the period of most rapid brain growth. Correcting this imbalance, the review argues, is one of the most pressing unanswered questions in the care of preterm infants.

Clinical trials are beginning to test that proposition directly. A randomized controlled trial led by researchers including Álvarez and colleagues examined early enteral supplementation with both arachidonic acid and DHA in very preterm infants, seeking to replicate in the nursery what the placenta would have delivered in utero. Complementary work by David Ramiro-Cortijo and colleagues assessed plasma oxidative status in preterm infants receiving LCPUFA supplementation, probing whether the fatty acids also modulate the oxidative stress that contributes to white matter injury. The commentary weaves these strands together to argue that the perinatal period—spanning pregnancy and the weeks after preterm birth—represents a continuous window of nutritional vulnerability and opportunity.

The authors are careful to frame their argument as a hypothesis-generating commentary rather than a definitive prescription. The observational studies linking nutrition programs to reduced cerebral palsy risk cannot fully disentangle nutrition from the many other advantages that come with program participation, including prenatal care, social support and reduced poverty-related stress. Season-of-conception analyses, which have found cerebral palsy risk varying with the time of year a pregnancy begins, hint at environmental and nutritional influences but likewise stop short of proving causation. What the commentary does establish, its authors contend, is that the convergence of epidemiology, animal neurobiology and early clinical trials now warrants rigorous intervention studies designed specifically to test whether optimizing maternal nutrition, including LCPUFA intake, can lower the incidence of cerebral palsy.

The implications reach well beyond the neonatal intensive care unit. If even a fraction of cerebral palsy risk is modifiable through diet, the public health payoff of ensuring adequate nutrition during pregnancy could be enormous, particularly in populations where food insecurity remains common. The WIC findings suggest that broad nutritional support programs may already be delivering neurodevelopmental benefits that were never part of their original design. For the Madrid team, the next step is to move from association to intervention: well-powered trials that measure not just birth outcomes but long-term neurodevelopment, and that treat the fatty acid composition of the maternal and infant diet with the same precision now applied to vaccines or antenatal steroids. The fetal brain, they argue, is built from what the mother eats—and medicine is only beginning to take that literally.

Subject of Research: The role of maternal nutrition and long-chain polyunsaturated fatty acids in fetal brain development and cerebral palsy prevention

Article Title: Adequate nutrition during pregnancy including LCPUFAs: a commentary

Article References: Saenz de Pipaon, M., Witte Castro, A., & Arribas Castaño, A. (2026). Adequate nutrition during pregnancy including LCPUFAs: a commentary. Pediatric Research. https://doi.org/10.1038/s41390-026-05575-3

Image Credits: AI Generated

DOI: 10.1038/s41390-026-05575-3

Keywords: maternal nutrition, cerebral palsy, LCPUFAs, DHA, arachidonic acid, preterm birth, fetal brain development, WIC program, neuroprotection, omega-3 fatty acids, neonatology, Pediatric Research