Fatty diet plays role in infant mental function
caused by prolonged seizures in newborn brain cells, says a team of
US researchers.
A high-fat diet may explain the better protection from damage caused by prolonged seizures in newborn brain cells, says a team of US researchers.
Their study on infant rats suggest that the high-fat diet of newborns, and the related increased production of a specific protein, protects their brain cells from damage that otherwise may accompany prolonged seizures. The finding may lead to new strategies to prevent brain injury in adults, said the scientists.
Seizures affect one in every 25 infants and children and over 1 per cent of all adults, where they may be associated with progressive loss of brain volume. Therefore, understanding how the immature brain prevents seizure-induced cell injury or death could point the way for researchers to develop new strategies aimed at preventing such damage in the mature brain.
In a study published in the online issue of the Annals of Neurology, Dr Tallie Z. Baram and her team found very high levels of a protein called uncoupling protein 2 (UCP2) in the brains of newborn rats. UCP2 production is stimulated by fatty acids. This high level of UCP2 may provide the protection from brain damage seen in infants who have seizures.
In the mature brain, seizures and other trauma kill and damage nerve cells by interfering with structures called mitochondria. Popularly referred to as 'the energy factories of cells', these cellular structures shuttle compounds back and forth during metabolic processes to produce energy.
"However a seizure can 'rev up' brain cells and their corresponding demand for fuel. The energy assembly line cannot keep up with this demand, the system gets jammed, reactive oxygen compounds form, and the cell is injured or dies," said Baram.
Surprisingly, the neonatal and immature brain seems to be immune to this damage.
Baram and her colleagues hypothesized that uncoupling proteins - specifically UCP2 found in mitochondrial membranes - reduce the formation of reactive oxygen compounds and decrease the potential for cell injury in the brains of immature rats. They found that UCP2 function and levels were significantly greater in immature animals. UCP2 production is increased by fatty acids, the breakdown products of dietary fat, and rat pups obtain most of their nutrition from maternal milk, which is very rich in fat.
The protective actions of UCP2 may also help explain why the ketogenic high-fat diet works in human children to prevent or dramatically reduce seizures, Baram said. This diet is used to treat severe, medicine-resistant seizures in children.
Although some preliminary unpublished data suggest a high-fat diet enhances UCP2 levels in the brains of mature mice, fatty acids may be less influential on the brain chemistry of older animals.
"This critical issue obviously needs to be carefully evaluated," said Baram.
