Foetus Suffer Brain Problems When Mother Lack Vitamin C

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Foetal brain can have severe consequences due to maternal vitamin C deficiency during pregnancy that cannot be reversed by taking vitamin C after birth, according to the latest research published in the journal of Plos One.

It is estimated that approximately 10 to 20% adults worldwide are suffering from vitamin C deficiency.                                                        "Fetus brain damage and vitamin C deficiency"

“Even marginal vitamin C deficiency in the mother stunts the foetal hippocampus, the important memory centre, by 10-15 per cent, preventing the brain from optimal development,” says Professor Jens Lykkesfeldt. He heads the group of scientists that reached this conclusion by studying pregnant guinea pigs and their pups. Just like humans, guinea pigs cannot produce vitamin C themselves, which is why they were chosen as the model.

“We used to think that the mother could protect the baby. Ordinarily there is a selective transport from mother to foetus of the substances the baby needs during pregnancy. However, it now appears that the transport is not sufficient in the case of vitamin C deficiency. Therefore it is extremely important to draw attention to this problem, which potentially can have serious consequences for the children affected,” says Jens Lykkesfeldt.

This study has focused on mother’s life style and nutritional status during pregnancy. The damage to the brain of fetus is such that it cannot be recovered even if vitamin C is administered to the baby was said by the researchers.

This study was conducted on guinea pig pups by dividing them into two groups. They gave vitamin C to the one group and second group was considered as a control group. Researchers did not found any sign of improvement in pups that were fed vitamin C when the pups were two months old, which corresponds to teenage in humans.

Now researchers are trying to investigate that how early in the pregnancy vitamin C affects the brain of foetus.

People with low economic status who eat poorly – and perhaps also smoke – often suffer from vitamin C deficiency. Comparatively speaking, their children risk being born with a poorly developed memory potential. These children may encounter learning problems, and seen in a societal context, history repeats itself because these children find it more difficult to escape the environment into which they are born,” says Jens Lykkesfeldt.

He emphasises that if pregnant women eat a varied diet, do not smoke, and for instance take a multi-vitamin tablet daily during pregnancy, there is no reason to fear vitamin C deficiency.

“Because it takes so little to avoid vitamin C deficiency, it is my hope that both politicians and the authorities will become aware that this can be a potential problem,” concludes Jens Lykkesfeldt.

The abstract of this article is as follows:

While having the highest vitamin C (VitC) concentrations in the body, specific functions of VitC in the brain have only recently been acknowledged. We have shown that postnatal VitC deficiency in guinea pigs causes impairment of hippocampal memory function and leads to 30% less neurons. This study investigates how prenatal VitC deficiency affects postnatal hippocampal development and if any such effect can be reversed by postnatal VitC repletion. Eighty pregnant Dunkin Hartley guinea pig dams were randomized into weight stratified groups receiving High (900 mg) or Low (100 mg) VitC per kg diet. Newborn pups (n = 157) were randomized into a total of four postnatal feeding regimens: High/High (Control); High/Low (Depleted), Low/Low (Deficient); and Low/High (Repleted). Proliferation and migration of newborn cells in the dentate gyrus was assessed by BrdU labeling and hippocampal volumes were determined by stereology. Prenatal VitC deficiency resulted in a significant reduction in postnatal hippocampal volume (P<0.001) which was not reversed by postnatal repletion. There was no difference in postnatal cellular proliferation and survival rates in the hippocampus between dietary groups, however, migration of newborn cells into the granular layer of the hippocampus dentate gyrus was significantly reduced in prenatally deficient animals (P<0.01). We conclude that a prenatal VitC deficiency in guinea pigs leads to persistent impairment of postnatal hippocampal development which is not alleviated by postnatal repletion. Our findings place attention on a yet unrecognized consequence of marginal VitC deficiency during pregnancy.

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