August 29, 2007
FAMILY MEALS FOCUS #19
Interpreting the news and research about feeding and eating

Currently, heightened concern about child overweight is being focused on pregnancy. The "fetal overnutrition hypothesis"¹ contends that the seeds of later overweight are planted in the fetus by parents' high BMI, the mother's "excessive" obstetrical weight gain and/or delivering a large baby.

There is no doubt that more children today plot at or above the 95th BMI percentile than can be statistically predicted. As FMF #14 pointed out, data correlating high birth weight with child and adult "overweight" is a numbers and semantics construct that pathologizes what for many children is normal growth. Five percent of children normally plot at the 95th percentile or above. Those relatively large and normally growing infants continue to be relatively large at age 7 years and as adults. Relatively large mothers, and to a lesser extent, relatively large fathers normally tend to have relatively large babies. But as FMF #13 pointed out, for many children that normal largeness is classified as overweight or obesity, leading alarmed parents to restrict their infant's food intake, thereby creating the very problem they are trying to avoid.

Hold back on the alarums and excursions! Far and away the majority of evidence indicates that low birth weight is the real concern. Low birth weight correlates with increased hypertension,^2,3 adult cardiovascular disease, and type 2 diabetes.² Epidemiological studies worldwide demonstrate a relationship between poor fetal growth and increased susceptibility to insulin resistance, visceral obesity, type 2 diabetes and other features of the metabolic syndrome in adulthood. Pooled results from 150,000 pregnancies correlate a one kg (2.2 lb) increase in birth weight with a 10-20% lower risk of subsequent ischemic heart disease (hardening of the arteries).⁴

Other studies find a U-shaped relationship between birth weight and disease. Low birth weight (less than 2,500 g, or 5.5 lb) or high birth weight (more than 4,000 g, or 8.8 lb), as compared with birth weight between 2,500 and 4,000 g, was associated with slightly increased risk of type 2 diabetes.⁵

Extensive metabolic research highlights the risks associated with food restriction during pregnancy. That research suggests that the culprit linking low birth weight and subsequent disease is fetal exposure to high levels of glucorticoid, a hormone produced by the mother to stimulate gluconeogenesis,⁶ the conversion of protein (and other arcane substances),to glucose, or energy. Energy is the primary requirement of the fetus, and if the mother doesn't consume enough energy, her levels of glucocorticoid go up and she burns protein, including her own body tissue, to get it.

What does this mean? These low correlations and contradictory results are nowhere near convincing enough to support interference with nutrition during pregnancy. In fact, the results support encouraging pregnant women to eat as much as they are hungry for and gaining adequate amounts of weight. Food restriction and striving for stated weight-gain outcomes during pregnancy distorts eating attitudes and behaviors and is potentially harmful for the mother and the fetus (see FMF #17).

The guiding principle, as always, is do no harm. The "fetal overnutrition hypothesis" carries the potential for increasing women's concerns about child overweight beginning in pregnancy and exacerbates the risk of distorting feeding dynamics throughout the child's growing-up years. Mothers who are concerned about a child's weight tend to feed in a restrained fashion-they try to get the child to eat less food and less-appealing food than they wish.⁷ As discussed in FMF #12, restrained feeding with respect to both amounts and types of food clearly correlates with increased child overweight.

Reference List

1. Lawlor DA, Smith GD, O'Callaghan M, et al. Epidemiologic Evidence for the Fetal Overnutrition Hypothesis: Findings from the Mater-University Study of Pregnancy and Its Outcomes. Am. J. Epidemiol. 2007;165:418-424.

2. Barker DJ, Eriksson JG, Forsen T, Osmond C. Fetal origins of adult disease: strength of effects and biological basis. Int J Epidemiol. 2002;31:1235-9.

3. Lawlor DA, Leon DA, Rasmussen F. Growth Trajectory Matters: Interpreting the Associations among Birth Weight, Concurrent Body Size, and Systolic Blood Pressure in a Cohort Study of 378,707 Swedish Men. Am. J. Epidemiol. 2007;165:1405-1412.

4. Huxley R, Owen CG, Whincup PH, et al. Is birth weight a risk factor for ischemic heart disease in later life? Am J Clin Nutr. 2007;85:1244-1250.

5. Harder T, Rodekamp E, Schellong K, Dudenhausen JW, Plagemann A. Birth Weight and Subsequent Risk of Type 2 Diabetes: A Meta-Analysis. Am. J. Epidemiol. 2007;165:849-857.

6. Stocker CJ, Arch JR, Cawthorne MA. Fetal origins of insulin resistance and obesity. Proc Nutr Soc . 2005;64:143-51.

7. Burdette HL, Whitaker RC, Hall WC, Daniels SR. Maternal Infant-Feeding Style and Children's Adiposity at 5 Years of Age. Arch Pediatr Adolesc Med. 2006;160:513-520.

Copyright © 2007 by Ellyn Satter. Published at www.EllynSatter.com.