While some genetic factors control growth and weight in both children and adults, those of most importance are actually different between children and adults and appear to change significantly over childhood, a study reports.
Its findings were published in the journal Nature Communications, in the paper “Genome-wide association study reveals dynamic role of genetic variation in infant and early childhood growth.“
It may seem logical to assume that, if a genetic variant has a particular effect – for example, predisposing a person toward a higher body weight – it would have that same effect at all stages of life. But human growth and development is complex.
Researchers used genetic data from a total of 17,474 children in the Norwegian Mother, Father, and Child Cohort Study, which recruited pregnant women in Norway from 1999 to 2008.
The children’s body mass index (BMI) was measured regularly over the course of nearly a decade: at birth, 6 weeks, 3, 6, and 8 months, and 1, 1.5, 2, 3, 5, 7, and 8 years of age. The study’s goal was to identify genes that affected the children’s weight over these early years of life.
“A better understanding of the biology of infant growth is important as growth-related diseases such as obesity and malnutrition are global societal challenges,” Pål Rasmus Njølstad, a professor at the University of Bergen and study co-author, said in a press release.
The researchers looked for statistically significant associations between genetic variants and the children’s BMI. It should be noted that BMI is just a ratio of weight and height that is not necessarily reflective of fat distribution or overall health; however, in large population studies like this, it is generally considered safe to assume that higher BMIs are suggestive of being overweight or obese.
They found several genetic variants that were strongly associated with BMI very early in life, but less so later on. These variations were primarily found in genes related to the leptin system; leptin is a hormone that is important for the regulation of appetite.
For example, a variation (rs2767486) in the LEPR gene that encodes the leptin receptor was significantly associated with BMI between the ages of 6 months and 1 year, but less so at other time points. Other variants in the ADCY3, LCORL, and LEP genes were associated with obesity at later timepoints, particularly between 1 and 2 years old.
Another variant in the fat mass and obesity-associated (FTO) gene (rs9922708) — a gene that has been extensively associated with adult obesity — showed a significant association at age 7.
“The study suggests that increased levels of leptin’s binding partner, the leptin receptor, in infants have a positive effect on weight gain without being linked to overweight in adults,” Njølstad said, adding, “This finding provides a potential target for drug intervention to increase weight in infants who need it.”
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