March 20, 2013
Starting An Infant On Solids Too Soon May Program Obesity For Life
Alan McStravick for redOrbit.com - Your Universe Online
In the United States, the struggle with obesity has been affecting more and more people with each succeeding year. The tax on our health care system with each new diagnosis of type 2 diabetes and endometrial cancer is increasingly evident. And according to a study released last year by the Trust for America´s Health and the Robert Wood Johnson Foundation, a full 50 percent of adults in the US could be classified as obese by 2030.While it would be easy to throw the blame squarely at the hard-to-be-seen feet of the overweight individual, the cause of and answer for this problem may not be as simple as putting down the fork. A new study out of the University of Buffalo (UB) School of Medicine and Biomedical Sciences claims that the metabolic programming of an individual may be set by the age of 4 months.
“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,” according to lead study author Mulchand S. Patel, PhD, the SUNY Distinguished Professor of Biochemistry and associate dean for research and biomedical education at UB. Their study, originally published online in December, has been published this month in the American Journal of Physiology: Endocrinology and Metabolism.
The study relied on research conducted with animal subjects and contends the consumption of foods high in carbohydrates immediately after birth plays an important role in programming the individual for a lifelong struggle with excess weight gain and, ultimately, obesity. This holds true even when the researchers restricted caloric intake in the adulthood of the animals.
“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 Patel. He claims the results of his research have applications to the obesity epidemic in the US, particularly as it relates to infant nutrition.
“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.”
Patel and his UB colleagues have, for more than 20 years, studied how the increased intake of carbohydrate-enriched calories just after birth can effectively be responsible for programming the individual to overeat throughout their lives.
The method employed by the team involved providing newborn rat pups special milk formulas developed to be similar to rat milk in its composition, with a higher fat-derived caloric content. Conversely, the second formula was 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.”
After three weeks, those rats raised on the high-carbohydrate formula were then weaned onto solid rat chow. Some rats were allowed either free access to the chow while others were placed on a moderated caloric restriction meant to mirror the level of consumption of those pups reared naturally.
“When food intake for the [high-carbohydrate formula] 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. “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 [high-carbohydrate formula] 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.
The suppression of the programming, rather than its eradication, is due to developmental plasticity. Developmental plasticity extends from fetal development into the immediate postnatal period. Patel alludes to previous research noting it had revealed 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,” states Patel. “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.”
Patel and his colleagues claim the results of their study point to the need to implement a permanent caloric restriction for individuals, rather than engaging in quick-fix diet regimens. In order to address the obesity epidemic in the US, a true lifestyle change must be undertaken.
“As long as you restrict intake, you can maintain normal body weight,” he says.
The team advises parents wishing to avoid a lifelong metabolic reprogramming that will predispose their child to obesity throughout their life to follow the American Academy of Pediatrics guidelines. These guidelines state solid foods should not be given before a baby is 4-6 months old.
Patel and his colleagues, recognizing this current study involved only moderate caloric restriction, claim they would like to study the implementation of a more severe caloric restriction over a limited period of time. Namely, they want to explore whether doing this might result in a true metabolic reprogramming resulting in a more normal metabolic phenotype.
Along with Patel, the study was co-authored by Malathi Srinivasan, PhD, a research assistant professor and Saleh Mahmood, PhD, a post-doctoral associate. Both Srinivasan and Mahmood are also in the UB Department of Biochemistry.
The work was supported by the National Institute for Diabetes and Digestive and Kidney Diseases.