Vitamin C deficiency in early postnatal life impairs spatial memory and reduces the number of hippocampal neurons in guinea pigs.
Level 5 - mechanism / opinion, no new human data
Animal experiment (guinea pigs).
PubMed 19640959 · doi:10.3945/ajcn.2009.27954
What was done
Thirty 6- to 7-day-old newborn guinea pigs were randomly assigned to two groups for two months: one receiving a vitamin C-sufficient diet and the other a low vitamin C diet adequate to prevent scurvy but induce chronic deficiency. Spatial memory was evaluated using the Morris Water Maze, and hippocampal neuron numbers in subdivisions (dentate gyrus, CA1, and CA2-3) were quantified using stereologic methods.
What was found
Compared with controls, vitamin C-deficient guinea pigs demonstrated impaired spatial memory (P < 0.05) and a significantly increased time to first platform hit (P < 0.05). Deficient animals also showed a lower total number of neurons across the dentate gyrus, CA1, and CA2-3 regions of the hippocampus (P < 0.05). Specific numerical counts, latencies, and effect sizes were not provided in the abstract.
Why it matters
This study shows that moderate vitamin C deficiency during early postnatal development can cause structural brain alterations and cognitive deficits in a species that cannot synthesize vitamin C endogenously.
Limits
The study is restricted to an animal model (n = 30 guinea pigs), limiting direct clinical translation to human infants. The abstract omits precise quantitative measurements, variance, and baseline nutritional parameters, reporting only P-value thresholds.
Cited by
- supports Studies in newborn guinea pigs demonstrated that prenatal and postnatal vitamin C deficiency stunted hippocampal development by 10% to 30%.