Maternal protein intake during pregnancy and offspring overweight 20 y later.
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Bech, Bodil H
Henriksen, Tine B
Rasmussen, Morten A
Olsen, Sjurdur F
Halldorsson, Thorhallur I
MetadataShow full item record
CitationAm. J. Clin. Nutr. 2014: 1-10
AbstractAnimal studies have shown that protein intake in pregnancy may influence offspring fat metabolism and adiposity. The macronutrient ratio in human pregnancy appears to be important for offspring glucose tolerance; however, less is known about the influence on offspring adiposity.
We examined the relation between maternal dietary protein intake during pregnancy and offspring anthropometric measures and biomarkers of adiposity and glucose metabolism.
We used a prospective cohort of 965 Danish pregnant women recruited in 1988-1989 with offspring follow-up at 19-21 y. Macronutrient intake was collected in gestational week 30, and we divided protein according to its source (animal and vegetable including cereals). Offspring body mass index (BMI; in kg/m(2)) and waist circumference were recorded at follow-up (n = 695-697), and biomarkers were quantified in a subset (n = 443) of participants. We used multivariable linear and log-binomial regression to calculate effect estimates and 95% CIs for a 1:1-g substitution of carbohydrates for protein.
Offspring mean (±SD) BMI was 22.1 ± 3.3 and 22.8 ± 2.9 for women and men, respectively. The prevalence of overweight (BMI ≥25) was 16.9% for women and 19.1% for men. We showed that a 1:1-g substitution of animal protein for carbohydrates increased risk of BMI ≥25 in female [quartile 4 compared with quartile 1: risk ratio (RR): 3.36; 95% CI: 1.52, 7.42] and male (quartile 4 compared with quartile 1: RR: 2.22; 95% CI: 0.92, 5.35) offspring. These results appeared to be accounted for by protein from meat sources. The results could not be explained by postnatal risk factors.
Protein from animal sources, primarily meat products, consumed during pregnancy may increase risk of overweight in offspring; this association appeared to be stronger for female offspring. Because of the lack of information on postnatal exposure in this cohort, these results are hypothesis-generating and need to be replicating in other cohorts.
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RightsArchived with thanks to The American journal of clinical nutrition
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