When babies are deprived of oxygen in utero, brain damage can result. Researchers have found a connection between brain damage and a fatty acid molecule, which could spark new treatment protocols to reduce the risk of brain damage. According to the Scripps Research Institute, LPA (a fatty molecule) may be associated with messages moving to the brain cells of the fetus. These messages may be associated with brain damage caused by lack of oxygen. If animal studies are correct, it would spark new and exciting research aiming toward blocking messages that cause brain damage. 

When the fetal brain does not get enough oxygen, developmental issues may arise. These issues exist far beyond infant years. The most widely recognized cause of oxygen deprivation, or hypoxia, is smoking while pregnant, but other causes are known. Currently, there are no treatments available to stop negative side effects of hypoxia, so doctors and researchers are constantly on the lookout for a starting point for further research and the LPA research may be that starting point. 

According to researcher Dr. Jerold Chun, “Fetal brain damage from oxygen deprivation involves specific changes that are, surprisingly, mediated by this lipid signal called LPA.” He notes further that LPA signals and pathways can be altered with medications, so the finding is particularly important. 

Researchers found that hypoxia causes brain neurons to go wild. These neurons act like they are being overstimulated by LPA. If this is the case, LPA-inhibiting drugs could stop the neuron overload and reduce the risk of developmental problems in utero. 

Despite the research, doctors note that smoking during pregnancy is not safe. Smoking causes a lack of oxygen to the fetus, which can cause life-long problems and low birth weight. Other causes of hypoxia include physical trauma and blockage of blood to the fetus. 

Source: Keira Joann Herr, Deron R. Herr, Chang-Wook Lee, Kyoko Noguchi, and Jerold Chun. The Scripps Research Institute. 3 September, 2011.