How genomics can reduce growing childhood obesity
Children with genetic mutations such as MC4R, LEP, FTO, and POMC affect the intake of hunger and food are at greater risk of developing the obesity of early-infests.

In short
- In addition to lifestyle, genetic mutations can cause childhood obesity
- Children with genetic mutations like MC4R are at greater risk of obesity
- However, genetic tendency is only a possible risk marker
Childhood obesity is affected by many factors, especially from poor diet, genetics, lack of physical activity and underlying medical conditions. This increasing public health concern is connecting the increasing burden of non-communicable diseases.
A advisor in the Department of Endocrinology at Ramaiya Memorial Hospital, Dr. Manjannath PR highlighted the dangerous increase in obesity rates among the youth population.
He said, “The rate of obesity, especially in small population, has increased in the last few decades. More than 390 million children aged 5–19 were declared overweight in 2022. The number creates immediate health concerns for countries around the world,” he told India Today Digital.
Modern lifestyle changes, such as inactivity, increase in screen time, poor sleep patterns, ultra-selot high-calorie foods consumption, sugary drinks and large portions contribute to weight gain.
Dr. Manjunath said, “Staying inside and the increase in screen time has changed the physical activity, causing dull, weight gain habits.”
Doctors suggest that progress in genomic technology allows preliminary detection of obesity related disorders and enabling counseling for parents about risks.

“Childhood obesity arises from a complex interaction of factors, including poor diet, genetics, lack of physical activity, and underlying medical conditions. While lifestyle plays a major role, genetics also have a significant effect on obesity,” Dr. Ramesh Menon said, Associate Director of Personal Genomics and Genomic Medication.
Children with genetic mutations such as MC4R, LEP, FTO, and POMC affect the intake of hunger and food are at greater risk of developing the obesity of early-infests.
Genetic conditions such as the Predar-Vilti syndrome and Lawrence-Moon-Bidel syndrome inspire children to obesity with increased appetite and low metabolism.
To evaluate a child’s risk for weight gain, polygenic risk scores (PRS) are used, which collect genetic forecasts from many genes.
“These genetic factors can be both monozenic and polygenic. While FTO (linked to fat mass and obesity) genes are widely identified for genes such as obesity, LEP (leptin), MC4R (Melanocortin receptor 4), and others play a significant role in the development of obesity.”
Several studies have installed a clear link between high PRS and an enlarged body mass index (BMI). However, Dr. Menon said that genetic tendency for obesity is not a predetermined destiny, but a possible risk marker.
“The actual value of PRS lies in their ability to quickly identify children with risk, enabling active intervention,” he said.
Individual strategies can be made, combined with lifestyle and environmental factors. These strategies may include consultation for parents, customized nutrition scheme, targeted fitness resignation and ongoing health monitoring.
It is important to identify that genetic tendency is not destiny, experts agree. With the initial identity and sewn interventions, informed decisions can be made to deal with the problem of childhood obesity.