Genetic factors that raise obesity risk in adults seem to start taking effect from ages 4 to 6
An indicator of body fat, body mass index or BMI in infants, children, and adults is influenced by different genetic factors that change as we age, says study
The origins of obesity in adults lie in early childhood, says a team of scientists, who have discovered that some genetic factors associated with adult body mass index (BMI) - an indicator of body fat - start playing a role during childhood, from around the age of 4 to 6 years.
The international consortium of researchers also found that BMI in infants is influenced by a distinct set of genetic variants - referring to bits of DNA that differ from one person to the other - which play little role in determining a person’s weight in later life.
The findings, says the research team, suggest that different genetic factors control infant and child BMI. The researchers conclude that body mass index in infants, children, and adults is influenced by different genetic factors that change as we age.
In light of the obesity epidemic, these findings are important and could make it possible to intervene at this early age (4 to 6 years) to help prevent unhealthy weight gain in later life, says the study published in Science Advances.
“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. 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,” says senior author Professor Marjo-Riitta Jarvelin, from Imperial College London’s School of Public Health.
“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,” adds professor Jarvelin.
Obesity and overweight, according to the World Health Organization (WHO), are defined as abnormal or excessive fat accumulation that presents a risk to health. Both are considered major risk factors for a number of chronic diseases, including heart disease, diabetes, and cancer. A person with a BMI of 30 or more is generally considered obese. A person with a BMI equal to or more than 25 is considered overweight. In 2016, over 1.9 billion adults, 18 years and older, were overweight, and of them, over 650 million were obese, says the WHO. Further, over 340 million children and adolescents aged 5-19 were overweight or obese in 2016.
The current research was conducted as part of the Early Growth Genetics Consortium, which combines data from multiple genome-wide association studies to identify genetic markers or variants that are implicated in human development.
For the current study, the research team assessed BMI and growth rates from two weeks to 13 years of age of more than 22,000 children and compared these to variations in their genetic make-up. “This enabled us to identify common genetic markers associated with the peaks and troughs in BMI and their timings in childhood,” says the team.
The researchers explain that BMI does not remain constant, now does it follow a linear path throughout a person’s life, but instead has three distinct periods of change. After birth, BMI increases rapidly until the age of nine months, where it peaks before declining again until the age of 5 to 6 years old, and this is known as “adiposity (obesity) rebound timepoint.” After this, an individual’s BMI steadily increases until early adulthood. In previous studies, scientists have suggested that obesity rebound is a critical period that can determine obesity in later life and the results from the new research now help to explain those findings, says the team.
The research team also identified 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, explain the researchers, this genetic region is involved in controlling the activity levels of a hormone called leptin, which is produced by fat cells to reduce appetite. The new variant discovered in the study, however, does not appear to be associated with adult weight regulation, so its effects may be limited to infancy, the researchers add.
The analysis suggests there are distinct biological processes driving BMI in infancy compared to later in childhood and into adulthood. “We would like to further explore this variation in genetic make-up in infancy to better understand its role in development. If we can explain what is happening in early life, then we can start to understand why some people become obese, and some people don’t even though they are eating the same amount of calories. This may allow us to tackle the risk factors that are leading to the obesity epidemic,” says Professor Jarvelin.