Does the introduction of baby foods too early in life increase carbohydrate intake? And would eating American (commercial) baby foods boost insulin secretion and cause metabolic programming that in turn predisposes your child to obesity later in life? Many American baby foods and juices are high in carbohydrates, mainly simple sugars. The hypothesis of a new study examined consumption of foods high in carbohydrates immediately after birth to see whether it programs individuals for lifelong increased weight gain and obesity.
Picture a food bank handing out a bag of free baby food to a family living below the poverty level. Can beggars be choosers when it comes to what healthy baby foods to feed your child? And for those who can afford choices, what type of high carb foods most predispose babies to obesity later in life by re-programming their systems--both before birth and within the first year thereafter?
Working with laboratory rats, a University at Buffalo animal study has found, even if caloric intake is restricted in adulthood for a period of time the 'programming' predisposed the lab animals to obesity later in life. The research on laboratory animals is now published in print in the March, 2013 issue of the American Journal of Physiology, Endocrinology, and Metabolism. But it has been published online since December 2012.
Do high carbohydrates fed to babies increase their insulin output, thereby programming kids for lifelong increased weight gain and obesity?
Consumption of foods high in carbohydrates immediately after birth programs individuals for lifelong increased weight gain and obesity, a University at Buffalo animal study has found, even if caloric intake is restricted in adulthood for a period of time. “This is the first time that we have shown in our rat model of obesity that there is a resistance to the reversal of this programming effect in adult life,” explains Mulchand S. Patel, PhD. He's the SUNY Distinguished Professor of Biochemistry and associate dean for research and biomedical education at the University at Buffalo School of Medicine and Biomedical Sciences, according to the March 19, 2013 news release, "High-carb intake in infancy has lifelong effects, UB study finds," by Ellen Goldbaum.
“Many American baby foods and juices are high in carbohydrates, mainly simple sugars,” he says. “Our hypothesis has been that the introduction of baby foods too early in life increases carbohydrate intake, thereby boosting insulin secretion and causing metabolic programming that in turn, predisposes the child to obesity later in life.”
The research has applications to the obesity epidemic in the U.S., particularly as it relates to infant nutrition, Patel explains
For more than 20 years, Patel and his UB colleagues have studied how the increased intake of carbohydrate-enriched calories just after birth can program individuals to overeat. For their rat model of obesity, the UB researchers administered to newborn rat pups special milk formulas they developed that are either similar to rat milk in composition, (higher in fat-derived calories) or enriched with carbohydrate-derived calories.
“These pups who were fed a high-carbohydrate milk formula are getting a different kind of nourishment than they normally would,” explains Patel, “which metabolically programs them to develop hyperinsulinemia, a precursor for obesity and type 2 diabetes,” according to the March 19, 2013 news release by Ellen Goldbaum, "High-carb intake in infancy has lifelong effects, UB study finds."
At three weeks of age, the rat pups fed the high-carbohydrate (HC) formula were then weaned onto rat chow either with free access to food or with a moderate calorie restriction, so that their level of consumption would be the same as pups reared naturally. “When food intake for the HC rats was controlled to a normal level, the pups grew at a normal rate, similar to that of pups fed by their mothers,” Patel says in the news release. “But we wanted to know, did that period of moderate calorie restriction cause the animals to be truly reprogrammed? We knew that the proof would come once we allowed them to eat ad libitum, without any restrictions.
“We found that when the HC rat undergoes metabolic reprogramming for development of obesity in early postnatal life, and then is subjected to moderate caloric restriction, similar to when an individual goes on a diet, the programming is only suppressed, not erased,” he says in the news release. This is due to developmental plasticity, which extends from fetal development into the immediate postnatal period. According to Patel, previous research by others has revealed that during the immediate postnatal period, pancreatic islets and neurons continue to mature.
“That’s why an altered nutritional experience during this critical period can independently modify the way certain organs in the body develop, resulting in programming effects that manifest later in life,” Patel explains in the news release. “During this critical period, the hypothalamus, which regulates appetite, becomes programmed to drive the individual to eat more food. We found that a period of moderate caloric restriction later in life cannot reverse this programming effect.”
Addressing the obesity epidemic in the U.S. requires true lifestyle change, including permanent caloric restriction
“As long as you restrict intake, you can maintain normal body weight,” he says in the news release. To avoid metabolic reprogramming that predisposes a baby to obesity later in life, he explains that parents should follow the American Academy of Pediatric guidelines, which state that solid foods should not be given before a baby is 4-6 months old.
Patel explains, "Our hypothesis has been that the introduction of baby foods too early in life increases carbohydrate intake, thereby boosting insulin secretion and causing metabolic programming that in turn predisposes the child to obesity later in life." Patel adds that this study involved only moderate caloric restriction.
He and his colleagues would like to study whether or not more severe caloric restriction for a limited period can result in true metabolic reprogramming to normal metabolic phenotype. Co-authors with Patel are Malathi Srinivasan, PhD, research assistant professor and Saleh Mahmood, PhD, post-doctoral associate, both in the UB Department of Biochemistry. The NIH/National Institute of Diabetes and Digestive and Kidney Diseases supported the work.
Also check out another study's 2005 abstract, "Maternal hyperinsulinemia predisposes rat fetuses for hyperinsulinemia, and adult-onset obesity and maternal mild food restriction reverses this phenotype." In a still older study (with rats), artificial rearing of newborn female rat pups on a high-carbohydrate (HC) milk formula resulted in chronic hyperinsulinemia and adult-onset obesity (HC phenotype). Also, the maternal HC phenotype was transmitted to their progeny (2-HC rats) because of fetal development in the HC female rat.
The aims of the 2005 study were to investigate the fetal adaptations that predisposed the progeny for the expression of the HC phenotype in adulthood and whether the transfer of the HC phenotype to the progeny could be reversed by maternal food restriction. The conclusion of the study reported that this mild dietary restriction reversed their HC phenotype and also prevented the development of the HC phenotype in their progeny.
Ongoing studies are required to find out more about what not to feed infants and babies to help them maintain their maximum healthy potential, and how what a mother eats before the baby is born affects the offspring. But as far as feeding babies commercial, high-carb baby food including juices and sweet baby food desserts, the recommendation is to not feed solid commercial food in the first six months of life to prevent the baby's body from programming itself to secrete excess insulin. That's why further research is needed to confirm the hypothesis of the ongoing research.
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