It is obvious that pediatric obesity is a growing problem. However, compared to adult obesity, it is a relatively new problem. In a new article to be published in the Journal of Adolescent Health, it is pointed out that while childhood obesity has increased some 300 percent since 1960, most of that increase only began in the mid 1990s (1). This is well after the beginning of the climb of adult obesity, which started in the 1980s. Why the lag time? I believe it may have been caused by the amplification of any genetic predisposition to obesity by prenatal programming in the womb. That means you had to have obese mothers whose own hormonal changes and diet were altering the fetal programming of their children, thus amplifying their likelihood for obesity after birth.
This possibility makes sense based on results from another recent article that demonstrates that the lower the omega-3 fatty acid status in the mother, the more likely the child would be obese by the age of 3 (2). In this particular study, researchers found that by age 3 about 10 percent of the children were already obese. What they also analyzed was even though virtually all the women were consuming very low levels of omega-3 fatty acids during pregnancy, the higher the levels of the omega-3 fatty acids in mother’s diet, or her blood, and especially in the blood from the umbilical cord to the fetus, the lower the levels of obesity in the child three years later after birth.
Of course, lower levels of omega-3 fatty acids usually indicate higher levels of omega-6 fatty acids, giving rise to an unbalanced ratio of omega-3 to omega-6 fatty acids. This is why the highest correlation with increased childhood obesity was found with an increasing ratio of arachidonic acid to EPA and DHA in the blood of the mother and also in the umbilical cord of the fetus. This makes perfect sense since it is known from animal studies that the higher the omega-6 to omega-3 ratio in the diet of the mother, the greater the obesity in the offspring (3-5).
So if you want to begin to decrease childhood obesity, it is probably best to start in the womb of the mother with appropriate prenatal nutrition using appropriate levels of omega-3 fatty acids. This would prevent the fetal programming of the unborn child that would lead to rapid accumulation of excess body fat after birth. I think this makes a lot more sense than telling obese children to “eat less and exercise more” after their genetic expression has been altered in the womb. And if this makes sense, then doesn’t it also strongly suggest that feeding children more omega-3 and less omega-6 fatty acids after birth will silence the activation of ancient genes that make them fat and keep them fat (6).
- Lee H, Lee D, Guo G, and Harris KM. “Trends in body mass index in adolescence and young adulthood in the United States: 1959-2002.” J Adolescent Heath DOI:10.1016/jadolheath2011.04.019 (2011)
- Donahue SMA, Rifas-Shiman SL, Gold DR, Jouni ZE, Gilman MW, and Oken E. “Prenatal fatty acid status and child adiposity at age 3.” Am J Clin Nutr 93: 780-788 (2011)
- Korotkova M, Gabrielsson BG, Holmang, A, Larrson BM, Hanson LA, and Strandvik B. “Gender-related long-term effects in adult rats by perinatal dietary ratio of n-6/n-3 fatty acids.” Am J Physiol Regul Integr Comp Physiol 288: R575-579 (2005)
- Ailhaud G, Guesnet P, and Cannane SC. “An emerging risk factor for obesity: does disequilibrium of polyunsaturated fatty acid metabolism contribute to excessive adipose tissue development?” Br J Nutr 100: 461-470 (2008)
- Massiera L, Barbry P, Guesnet P, Joly A, Luquet S, Moreihon-Brest C, Moshen-Kanson T, Amri E-Z, and Ailhaud G. “A western-like fat diet is sufficient to induce a gradual enhancement in fat mass over generations.” J Lipid Res 51: 2352-2361 (2010)
- Massiera Saint-Marc P, Seydoux J, Murata T, Kobayshi T, Narumiya S, Guesnet P, Amri E-Z, Negrel R, and Alhaud G. “Arachidonic acid and prostacyclin signaling promote adipose tissue development: a human health concern?’ J Lipid Res 44: 271-279 (2003)
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