Genetic Risk Factors for Obesity Seen to Differ Between Children and Adults
Genetic risk factors underlying childhood obesity differ from those in adulthood, a large-scale analysis found.
Better understanding of such risk factors could further the study of childhood obesity in relation to health later in life.
The study, “Separating the genetics of childhood and adult obesity: a validation study of genetic scores for body mass index in adolescence and adulthood in the HUNT Study,” was published in the journal Human Molecular Genetics.
Many children with obesity carry excess weight into adulthood, leading to problems such as type 2 diabetes or cardiovascular disease.
However, the genetic factors that drive this process are not well understood. In addition, separating the impact of childhood obesity from factors underlying obesity that starts in adulthood is challenging.
To address this knowledge gap, a recent study in the U.K. used large-scale genetic analysis to calculate polygenic risk scores in different age groups.
A polygenic risk score indicates the risk of developing a disease in comparison with people with a different genetic constitution.
Results showed that childhood risk scores best predicted body mass index (BMI, a measure of body fat) at age 10, whereas adult risk scores were a strong predictor of adult BMI, suggesting that the genetic influence on obesity is distinct in childhood and adulthood.
Childhood risk scores calculated in the earlier study were derived from questionnaires given to adults, ages 40 to 69, about their body size at age 10. As such, they rely on the accurate recall of participants, said the investigators.
In an attempt to validate these risk scores, researchers in Norway and the U.K. extracted data from the ongoing HUNT study — a large-scale database containing questionnaire data, clinical measurements, and biological samples from people who live in a single Norwegian county.
The team, which included two researchers from the U.K. study, looked at data covering 66,963 people of European descent, ages 12 to 70, collected over six decades. Almost all participants with a BMI measurement taken before age 18 also had at least one BMI measurement taken as adults. Blood samples were collected for genetic analyses.
Only a moderate correction was seen between childhood and adult polygenic risks scores. Specifically, in the group of children between 12 and 15.9 years old, the variation explained by the childhood polygenic risk scores was 6.7% compared with 2.4% as calculated from adult risk scores.
In contrast, in the age group spanning 24 to 29.9, the variance explained by the adult risk scores was 3.9% versus 3.6% for the childhood scores.
Together, these results suggested that genetic factors underlying childhood obesity are different from those of adult obesity, and this change occurs in adolescence and early adulthood, the team said.
Consistently, further statistical analysis found that childhood scores were superior to the adult scores in predicting obesity in the age group 12 to 15.9. In contrast, there is no difference between the two scores in the 16 to 17.9 age range.
Also, the effect of the childhood risk score on BMI was relatively constant throughout life, while the impact of the adult risk score on BMI increased with age.
The BMI effect of the two scores overlapped when obtained in early adulthood, which implied that “neither score is better at predicting BMI in this age range,” the researchers wrote.
“Our findings support that genetic factors driving BMI differ at [a] young age and in adulthood,” they added. These findings also validate the U.K. study, in that “childhood polygenic risk score for BMI is a predictor of childhood obesity in the past and the present.”
“Validation of separate gene scores for adult and childhood BMI enables us to study childhood obesity and its relation to later health,” they wrote. “Using human genetics to disentangle the contribution of childhood and adult BMI to disease risk can be an attractive and cost-effective approach to help improve prevention strategies.”
Notably, genetic risks for childhood obesity are likely to vary between different ethnic groups, the investigators said.