Bottle-fed baby ‘prone to diabetes and obesity’.

Babies who are fed on inappropriate formula milk in the first weeks of life may be predisposed to obesity and diabetes in adulthood, research has revealed.

The research also suggests that women born in the 50s and 60s, who were fed formula milk as babies and have since become obese or diabetic, may be passing the condition on to their own children, whether they are breast or bottle-fed.

Mulchand Patel, Professor of Biochemistry at the University of Buffalo, New York, said: “Babies who were formula-fed when it was popular in the 1950s and 1960s may have developed obesity as adults and may have passed on this trait to their children.”

The study offers an insight into the causes of obesity, suggesting strongly that an infant’s diet sets a permanent pattern for the way in which the body responds to food.

Modern formula milk mimics the composition of breast milk more closely, and does not present a risk, but overfeeding or premature weaning could expose babies to excess carbohydrate and trigger high insulin and obesity.

“We are always looking at what happens later in life,” Professor Patel said. “Maybe we should be looking at the role of early metabolic programming. The results from this study involving the high-carbohydrate-fed rat model suggest that what foods human babies are fed may contribute to metabolic programming, leading to adult-onset diseases such as obesity and diabetes.

“Overfeeding of formula and early introduction of supplemental weaning foods such as cereals, fruits and juices that are high in carbohydrates may be the culprits.”

Breast feeding is the safest way to ensure that babies are given safe concentrations of carbohydrate, even though formula is now designed to have the same concentration as human breast milk – about 7 per cent. “With breast feeding, the mother produces an adequate amount of milk naturally,” Professor Patel said. “With formula feeding, the tendency is to finish the bottle, and this may result in overfeeding. It is evident from our studies that the composition and the timing of the dietary treatment programmes the onset of pathological conditions in adults that mimic major metabolic diseases noted in humans, such as obesity and type 2 diabetes.”

Maximum and minimum levels of carbohydrate in formula milk are controlled by law in Britain, with no more than 14 grams permitted per 100 kilocalories of energy.

In the Buffalo study, details of which were presented yesterday at the Experimental Biology conference in New Orleans, scientists discovered that rat pups fed milk containing too much carbohydrate developed abnormally high insulin levels and gained weight. Those changes persisted in later life, even with a normal diet. The effect, known as “metabolic programming”, also carried through to the next generation, with the offspring of female rodents that ate badly in infancy becoming prone to high insulin and obesity when reared on mother’s milk.

The specially modified milk formula for the rat pups was composed of 56 per cent carbohydrate, 20 per cent fat and 24 per cent protein. Normal rat milk contains just 8 per cent carbohydrate, 68 per cent fat and 24 per cent protein. The pups were fed the milk for 24 days, their natural suckling period, before being weaned.

Within 24 hours of receiving the formula milk, the pups developed raised insulin levels, which persisted throughout their lives, and they also gained weight, eventually becoming obese.

The diet had caused permanent changes in the rats’ pancreatic islet cells, which produce insulin, Professor Patel’s team found. The diet also provoked a knock-on effect on the next generation of rats: mothers reared on the formula produced offspring that had high insulin levels, even though the pups were fed on natural milk.

The effect was not transmitted through fathers reared on formula, suggesting that it is passed on in the womb or through milk.

© 2002 Times Newspapers Ltd.

Written by Mark Henderson, Science Correspondent for The Financial Times, and published on DrKelley.info, April 26, 2002. Embedded links (if any) may no longer be active. (Ed. 01.11.11)

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