Overview: The Pune Maternal Nutrition Study (PMNS) was set up prospectively in 1994 in six villages near Pune city. The women, who were recruited before pregnancy, were undernourished and did heavy farming work even when pregnant. The children are now aged 18 years.
Objective: The general objective was to explore associations between maternal nutrition and offspring birth outcomes and later cardiometabolic risk. Since 2012 this cohort study has become a randomised controlled trial, testing the effect of vitamin B12 supplementation of the adolescent children on outcomes in the next generation.
Methods: In the initial study, women’s pre-pregnancy anthropometry was measured, and serial data on their diet and micronutrient status were collected during pregnancy. Fetal growth was measured by ultrasound and detailed anthropometry was carried out at birth and annually during childhood (N=702). At 6 and 11 years, body composition, cardiometabolic risk factors and cognitive function were measured in the children and parents.
The study showed that children of B12 deficient mothers had higher insulin resistance. This and other findings led to the decision to convert the PMNS to an intervention study. The cohort has reached the age when they are beginning to marry and have their own children, and the adolescents are now enrolled in a trial to test the hypothesis that B12 supplementation, with and without additional micronutrients, will improve B12 status and reduce cardiometabolic risk in the next generation, acting through epigenetic mechanisms.
Research output and key findings in the last quinquennium: 16 published papers.
- Vitamin B12 deficiency and hyper-homocysteinaemia are common in this rural population, while folate deficiency is rare. B12 deficiency is due to low dietary intakes and not malabsorption, and can be remedied using a physiological daily dose of B12 (2µg) over 6-12 months17,164
- Maternal methyl-tetra-hydrofolate reductase (MTHFR) genotype is associated with both hyper-homocysteinaemia and low birthweight, suggesting a causal link between hyper-homocysteinaemia and reduced fetal growth [manuscript in press]