press release
Published: 05 September 2019

Genetic factors influencing adult obesity take effect in early childhood

By Natasha Meredith

Body mass index (BMI) in infants, children and adults is influenced by different genetic factors that change as we age, according to a major new study.

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They found, however, that some genetic variants associated with adult BMI start playing a role during childhood from around the age of 4-7 years old – suggesting that the origins of obesity in adults may lie in this critical stage of childhood.

The study, published in Science Advances, raises hopes that it may be possible to intervene at this early age to help to prevent unhealthy weight trajectories in later life.

“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,” said senior author Professor Marjo-Riitta Jarvelin, from Imperial’s School of Public Health.

“Environmental factors like the food we eat and our lifestyle have more and more impact on obesity development as we age. These external factors seem to unmask gradually the genetic contributors to obesity that we have from early life, programming development towards an unhealthy direction.

“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.”

The research was conducted as part of the Early Growth Genetics Consortium, which combines data from multiple genome-wide association studies to identify genetic variants implicated in human development.

In total, they analysed measures such as BMI and growth rates from 2 weeks to 13 years of age of more than 22,000 children and compared these to variations in their genetic make-up. This enabled the researchers to identify common genetic variants associated with the peaks and troughs in BMI and their timings in childhood.

BMI (an indicator of body fat) does not follow a linear path through a person’s life, but instead has three distinct periods of change. After birth, BMI rises rapidly until the age of nine months, where it peaks before declining again until the age of 5-6 years old, known as ‘adiposity rebound point’. BMI then steadily increases until early adulthood.

Previous studies have suggested that adiposity rebound is a key period for determining obesity in later life and the results from the new research now help to explain those findings.

The researchers also discovered a new genetic variant that has an effect on infant BMI, a variation in a region of the genome containing the genes LEPR and LEPROT. In adults this genetic region is involved in controlling the activity levels of a hormone called leptin which is produced by fat cells to reduce appetite. Evidence also suggests that in early life it plays a role in brain development.

This new variant unveiled in the study, does not appear to be associated with adult weight regulation, so its effects may be limited to infancy.

Dr Alex Couto Alves, Lecturer at the University of Surrey, and first author of the study, said: “Between the ages of five and seven years old, the genetic determinants of adult obesity start acting, highlighting a critical developmental window when intervention strategies to prevent and treat it could be implemented.

“Obesity has reached epidemic proportions, with 650 million obese and more than 1 billion adult’s overweight. This puts increased pressure on health services across the world to treat illnesses such as type 2 diabetes and cardiovascular disease which often develop due to obesity. It is important we tackle this at an early stage.”

Inga Prokopenko, Professor e-One Health and Head of Statistical Multi-Omics at the University of Surrey, added: “Rare coding DNA variants in LEPR gene leading to loss of respective protein function are related to the rare forms of severe obesity in children. This study highlights the role of common variants located in the non-coding sequence of LEPR/LEPROT genes and provides us with novel insights about the role of such DNA variation in influencing leptin-melanocortin signalling during early childhood”.

Dr Marika Kaakinen, Lecturer in Statistical Multi-Omics at the University of Surrey and a co-author of the study: “I started working with these data more than ten years ago by designing and coordinating the extraction of the growth data from the medical health records of the Northern Finland Birth Cohorts included in the study. For me it is absolutely wonderful to see the biological insights the analyses provided us with, based on these very unique and valuable data.”



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