Affiliation:
1. National Institute of Diabetes and Digestive and Kidney Diseases
2. NIDDK/NIH
3. National Institutes of Health
4. NIDDK, Phoenix, AZ
Abstract
Abstract
Background/Objectives: Lower birthweight has been previously identified as a risk factor for multiple chronic diseases which are also associated with poor diet. We sought to determine whether birthweight is related to objectively measured energy intake in adulthood. We hypothesized a negative association between birthweight and overall energy intake in adulthood.
Subjects/Methods: Healthy Indigenous American adults (n=65; age 33.2±8.0 years; female n=29; BMI 33.2±8.1 kg/m2) with measures of birthweight (mean 3465±376g; mean gestational age 40.1±1.2 weeks), ad libitum energy intake, and body composition were included. Three-day energy intake was measured using vending machines and categorized as high (≥45% kcal) or low in fat (<20% kcal) and as high in complex-carbohydrates (≥30% kcal), simple-sugars (≥30% kcal), or protein (≥13% kcal). Body composition was measured by DXA. General linear models assessed relationships between birthweight and intake, including age, sex, sex-birthweight interactions, fat mass index, and fat-free mass index as covariates.
Results: A birthweight-by-sex interaction was found such that birthweight was associated with energy intake negatively in males and positively in females (interaction p=0.04; simple slopes: male β=−64, female β= 93 kcal/day per 100 g birthweight). This pattern was evident in fat (interaction p=0.01; simple slopes: male β=−48, female β=42 kcal/day per 100g birthweight), protein (interaction p=0.02; simple slopes: male β=−5, female β=20 kcal/day per 100g birthweight), and high-fat/high-protein (interaction p=0.01; simple slopes: male β=−46, female β=45 kcal/day per 100g birthweight) consumption.
Conclusion: Birthweight was negatively associated with energy intake in adult males but was positively associated with energy intake in adult females.
Publisher
Research Square Platform LLC
Reference38 articles.
1. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis;Hales CN;Diabetologia,1992
2. Organ-selective growth in the offspring of protein-restricted mothers;Desai M;British Journal of Nutrition,1996
3. The developmental origins of the metabolic syndrome;Gluckman PD;Trends in Endocrinology & Metabolism,2004
4. The thrifty phenotype hypothesis: Type 2 diabetes;Hales CN;British medical bulletin,2001
5. McMillen IC, Muhlhausler B, Duffield J, Yuen B. Prenatal programming of postnatal obesity: fetal nutrition and the regulation of leptin synthesis and secretion before birth. Proceedings of the Nutrition Society. 2004;63(3):405 – 12.