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How nutrition in early life affects adult bone health

The University of Auckland
30 August 2017

How nutrition in early life affects adult bone health

We have all heard that a high-fat diet raises your risk for heart disease and metabolic diseases such as type 2 diabetes in adulthood. Now new research shows it also compromises your bone health, especially if you were born small or early, or if your mother had poor nutrition during pregnancy.

Researchers from the Liggins Institute and the University of Auckland analysed the bone structure of rats whose mothers were either fed normally or undernourished during pregnancy. Half of the rat offspring from each group of mothers were then fed a regular diet from weaning, the other half were fed a high-fat diet.

Compared to the other groups, the bones of the rats in the undernourished-mother-plus-high-fat-diet group had the lowest bone mineral content and fewer, more widely spaced bone plates – characteristics of reduced bone strength.

Past animal studies have shown that poor nutrition in pregnant mothers “programmes” the metabolism of their children in a way that raises their risk of later developing overweight and obesity. This study is the first to uncover a compounding effect of poor maternal nutrition and a high-fat diet in offspring on later bone health.

“This may have implications for thousands of children around the world, whose mothers have poor nutrition due to forces such as poverty and the obesogenic environment, and then who are exposed to high-fat Westernised diets in childhood,” says study lead Professor Elwyn Firth, at the Liggins Institute and the Department of Exercise Sciences at the University of Auckland. “Other research shows kids with obesity are prone to fractures, and that osteoporosis in older people has its origins in young (fetal or postnatal) life.”

The research team also investigated what changes in the early environment did to later bone health. Prior research from the Liggins Institute has shown that treating offspring with the obesity-related hormone leptin, a hormone that regulates appetite and energy balance, can reverse metabolic programming, so that offspring grow up with normal body weight, fat mass and leptin levels.

What they found was striking: if new-born rats born to undernourished mothers and then fed a high-fat diet were treated with leptin for 10 days, the programming effects on bone structure were permanently reduced or even reversed.

But the same leptin treatment given to new-born rats on a high-fat diet whose mothers had eaten a regular diet had a negative effect on bone health – it reduced bone length. This means leptin reversed the effect of the mother’s malnutrition, but not the effect of the offspring’s own poor diet.

“At the moment, leptin is not a viable treatment option for babies, because we do not yet know what the safe levels are, and evidence like this suggests it could be detrimental for babies who are not low in leptin,” says Dr Elwyn Firth.

“Leptin is not a treatment option for most adults with obesity, as they are less sensitive than normal to this hormone,” says co-researcher Professor Mark Vickers at the Liggins Institute.

“But our study opens up other possible therapeutic avenues for children and once again highlights the importance of early life for optimising health later in life. We already know from our previous research that exercise early in life can improve bone health and strength into adulthood.

“It’s also known that maintaining a certain leptin level in early life is essential for normal regulation of metabolism, and that food and exercise affect leptin levels. Perhaps in the future it will be possible to change leptin levels without an injection, by using nutrition and exercise, which may counteract the programming effects.”

The team’s next step will be to test different doses of leptin in rats, and investigate how exercise in early life affects leptin levels and adult bone health.

The other researchers in the team were Greg Gamble and Professor Jillian Cornish from the Bone and Joint Research Group at the University of Auckland’s Department of Medicine.

Says Dr Firth, “Our study points to a deepening understanding of the skeleton as not only a structural organ, but as part of the hormonal system, which in turn powerfully influences metabolism. And metabolism – what you do with energy from diet – is the crux of why some children and adults become overweight or obese.”

The findings were published in Scientific Reports.

ENDS

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