To examine if smaller size at birth, an indicator of growth restriction in utero, is associated with lower cognition in late life, and whether this may be mediated by impaired early life brain development and/or adverse cardiometabolic programming.

Longitudinal follow-up of a birth cohort.

CSI Holdsworth Memorial Hospital (HMH), Mysore South India.

721 men and women (55–80 years) whose size at birth was recorded at HMH. Approximately 20 years earlier, a subset (n = 522) of them had assessments for cardiometabolic disorders in mid-life.

Standardized measurement of cognitive function, depression, sociodemographic, and lifestyle factors; blood tests and assessments for cardiometabolic disorders

Participants who were heavier at birth had higher composite cognitive scores (0.12 SD per SD birth weight [95% CI 0.05, 0.19] p = 0.001) in late life. Other lifecourse factors independently positively related to cognition were maternal educational level and participants’ own educational level, adult leg length, body mass index, and socioeconomic position, and negatively were diabetes in mid-life and current depression and stroke. The association of birth weight with cognition was independent cardiometabolic risk factors and was attenuated after adjustment for all lifecourse factors (0.08 SD per SD birth weight [95% CI −0.01, 0.18] p = 0.07).

The findings are consistent with positive effects of early life environmental factors (better fetal growth, education, and childhood socioeconomic status) on brain development resulting in greater long-term cognitive function. The results do not support a pathway linking poorer fetal development with reduced late life cognitive function through cardiometabolic programming.

There is evidence that subclinical vitamin B12 (B12) deficiency is common in India. Vegetarianism is prevalent and therefore meat consumption is low. Our objective was to explore the contribution of B12-source foods and maternal B12 status during pregnancy to plasma B12 concentrations.

Maternal plasma B12 concentrations were measured during pregnancy. Children’s dietary intakes and plasma B12 concentrations were measured at age 9·5 years; B12 and total energy intakes were calculated using food composition databases. We used linear regression to examine associations between maternal B12 status and children’s intakes of B12 and B12-source foods, and children’s plasma B12 concentrations.

South Indian city of Mysore and surrounding rural areas.

Children from the Mysore Parthenon Birth Cohort (n 512, 47·1 % male).

Three per cent of children were B12 deficient (<150 pmol/l). A further 14 % had ‘marginal’ B12 concentrations (150–221 pmol/l). Children’s total daily B12 intake and consumption frequencies of meat and fish, and micronutrient-enriched beverages were positively associated with plasma B12 concentrations (P=0·006, P=0·01 and P=0·04, respectively, adjusted for socio-economic indicators and maternal B12 status). Maternal pregnancy plasma B12 was associated with children’s plasma B12 concentrations, independent of current B12 intakes (P<0·001). Milk and curd (yoghurt) intakes were unrelated to B12 status.

Meat and fish are important B12 sources in this population. Micronutrient-enriched beverages appear to be important sources in our cohort, but their high sugar content necessitates care in their recommendation. Improving maternal B12 status in pregnancy may improve Indian children’s status.

We aimed to test the fetal overnutrition hypothesis by comparing the associations of maternal and paternal adiposity (sum of skinfolds) with adiposity and cardiovascular risk factors in children.

Children from a prospective birth cohort had anthropometry, fat percentage (bio-impedance), plasma glucose, insulin and lipid concentrations and blood pressure measured at 9·5 years of age. Detailed anthropometric measurements were recorded for mothers (at 30 ± 2 weeks’ gestation) and fathers (5 years following the index pregnancy).

Holdsworth Memorial Hospital, Mysore, India.

Children (n 504), born to mothers with normal glucose tolerance during pregnancy.

Twenty-eight per cent of mothers and 38 % of fathers were overweight/obese (BMI ≥ 25·0 kg/m2), but only 4 % of the children were overweight/obese (WHO age- and sex-specific BMI ≥ 18·2 kg/m2). The children's adiposity (BMI, sum of skinfolds, fat percentage and waist circumference), fasting insulin concentration and insulin resistance increased with increasing maternal and paternal sum of skinfolds adjusted for the child's sex, age and socio-economic status. Maternal and paternal effects were similar. The associations with fasting insulin and insulin resistance were attenuated after adjusting for the child's current adiposity.

In this population, both maternal and paternal adiposity equally predict adiposity and insulin resistance in the children. This suggests that shared family environment and lifestyle, or genetic/epigenetic factors, influence child adiposity. Our findings do not support the hypothesis that there is an intra-uterine overnutrition effect of maternal adiposity in non-diabetic pregnancies, although we cannot rule out such an effect in cases of extreme maternal obesity, which is rare in our population.