Maternal vitamin C deficiency during pregnancy persistently impairs hippocampal neurogenesis in offspring of guinea pigs.
Level 5 - mechanism / opinion, no new human data
Animal research model
PubMed 23119033 · doi:10.1371/journal.pone.0048488
What was done
Eighty pregnant Dunkin Hartley guinea pig dams were randomized to diets with High (900 mg/kg) or Low (100 mg/kg) vitamin C. Newborn pups (n = 157) were randomized into four postnatal diet groups: High/High (Control), High/Low (Depleted), Low/Low (Deficient), and Low/High (Repleted). Postnatal hippocampal volume was measured with stereology, and newborn cell proliferation, survival, and migration in the dentate gyrus were assessed using BrdU labeling.
What was found
Prenatal vitamin C deficiency significantly reduced postnatal hippocampal volume (P<0.001), and postnatal repletion did not reverse this effect. Postnatal cell proliferation and survival rates in the hippocampus showed no difference between dietary groups, but migration of newborn cells into the granular layer of the dentate gyrus was significantly reduced in prenatally deficient animals (P<0.01). Absolute volumes and cell counts were not reported in the abstract.
Why it matters
The findings show that maternal vitamin C deficiency during gestation causes persistent structural impairment in offspring hippocampal development that cannot be corrected by postnatal supplementation.
Limits
The study was conducted in guinea pigs, and findings cannot be directly assumed for human development. The abstract provides P-values but lacks absolute values, effect sizes, and behavioral or memory testing in the offspring.
Cited by
- supports Studies in newborn guinea pigs demonstrated that prenatal and postnatal vitamin C deficiency stunted hippocampal development by 10% to 30%.