The genetic factors influencing weight do not remain the same throughout a person’s life, according to a large genome-wide analysis of early growth traits.
In babies, the set of genetic variants determining body mass index (BMI, a measure of body fat) plays no part in adult obesity. But interestingly, some variants associated with adult obesity also affect weight in early childhood, suggesting that obesity may start at this early stage in development.
“GWAS on longitudinal growth traits reveals different genetic factors influencing infant, child, and adult BMI” was published in the journal Science Advances.
The way the body accumulates fat changes as we age, particularly in very early life. Generally, this follows a trend with three stages: first, up to the age of about 9 months, bodies accumulate more and more fat. This is called the “adiposity peak.” Then, until around 5 or 6 years of age, proportional body fat decreases, which is called the “adiposity rebound.”
After the adiposity rebound, bodies tend to gradually put on more fat until after puberty, typically plateauing in early adulthood.
However, whether specific genetic factors influence these changes at different stages of development is unknown.
Researchers analyzed data from more than 22,000 children of European ancestry. The data — mostly garnered in previous studies — included genetic variations and growth data (height, weight, etc.) between the ages of 2 weeks and 13 years.
The researchers compared genetic variants to the children’s BMI — a ratio of weight to height that can be used to estimate body fat composition — at three time points: infancy (at adiposity peak), early childhood (at adiposity rebound), and afterwards (broadly defined as adult BMI).
They identified dozens of genetic variants that were significantly associated with adult BMI, and many of these also significantly associated with BMI in early childhood.
“Our study shows that nearly 100 genetic variants which increase a person’s risk of obesity in adulthood seem to start taking effect at an important stage of childhood development, from the age of around four,” Marjo-Riitta Järvelin, MD, MSc, PhD, FFPM, a professor at Imperial College London and co-author of the new study, said in a university news story by Ryan O’Hare.
However, the genetic variants that were linked to BMI at adiposity peak were different from those in childhood or adulthood. For instance, a variation (called rs9436303) in the gene that codes for leptin, an appetite-regulating hormone, explained about 0.3% of BMI variance in infancy — but this variant wasn’t significantly associated with BMI at adiposity rebound or adult BMI.
This finding, Järvelin said, “suggests there are distinct biological processes driving BMI in infancy compared to later in childhood and into adulthood.”
Broadly, these findings suggest that genetic predispositions toward obesity start having an impact fairly early in life, if not right out of the womb. This, in turn, suggests that early childhood — around the time of adiposity rebound — may be a critical time for interventions aimed at preventing obesity in those with a strong genetic risk.
“We have shown that the origins of adult obesity lie in early childhood, and that there are clear windows across the life course which should be better considered in obesity prevention,” Järvelin said.