Eating Habits, Activity at Home Matter for Kids at Genetic Risk of Obesity

Eating Habits, Activity at Home Matter for Kids at Genetic Risk of Obesity

A home environment that promotes obesity, such as eating unhealthy food, doing less exercise, and having more sedentary behaviors, makes children at risk for genetic obesity more vulnerable to excessive weight gain, according to a study. 

This susceptibility was significantly lower in children who carried a genetic risk but were raised in healthier environments.

Thus, adopting healthier food habits and promoting more physical activity can be particularly important to offset a child’s genetic risk for obesity, researchers say.

The study, “Variation in the Heritability of Child Body Mass Index by Obesogenic Home Environment” was published in the journal JAMA Pediatrics.

It was also the focus of the journal’s editorial, titled “Healthy Homes and Obesogenic Genes in Young Children.

It is well-established that childhood obesity is heritable, with a significant portion of the child’s weight attributed to genetic risk factors transmitted by the parents.

But important questions remain unanswered, as highlighted by the editorial: To what extent do certain environmental factors reliably amplify or attenuate genetic influences on child weight status? Can healthier environments in fact offset obesogenic genes?

Understanding how the interaction between genes and environment affects obesity has the potential to inform new prevention strategies and personalized treatments for addressing this condition.

Researcher Clare Llewellyn’s Obesity Research Group at University College London was interested in addressing this interaction.

They explored a prior line of work showing that preschool children who lived in “higher-risk home environments” had poorer diets, less physical activity, and watched more television than did children who lived in “lower-risk home environments.”

This study was the first to test the behavioral susceptibility theory, which proposes that heritability of body mass index (BMI) is higher among children who live in higher-risk home environments.

Researchers looked at relationships between home environment and BMI SD scores, or Z-scores, of 4-year-old twins. BMI SD scores are one of the most widely used methods to compare the weight of a child to the population reference.

Both identical (monozygotic) and fraternal (dizygotic) twins were used to assert the influence of genetics versus environment. The contribution of each for variation in a trait — in this case BMI — can be estimated by comparing similarity between identical twins (who share the same genetic makeup) with that between fraternal twins (who share approximately 50% of their genes).

The team looked at data from 925 twin pairs born in England and Wales during 2007, registered in the Gemini cohort, a U.K. study assessing the genetic and environmental influences on childhood excess weight gain.

Parents completed an initial questionnaire when their children were a mean 8.4 months old and then took part in another interview — the Home Environment Interview (HEI) — when their children were around age 4.

This interview is considered a rigorous assessment of food habits (e.g. availability of healthy and unhealthy foods, parental feeding practices), opportunities for physical activity and media-related behaviors (e.g. hours watching TV, household rules concerning media use) of each family.

Each item was rated with a score, and the sum of all was used to create an overall obesogenic risk score.

Families above mean score were considered to have a “higher-risk environment,” whereas those below that mean were classified as a “lower-risk home environments.”

Based on the data, researchers estimated that BMI heritability was 86% among children raised in homes with higher obesogenic risk, compared with 39% for those living in lower-risk home environments. 

“The impact of genetic factors thus was curbed by roughly half in a healthier environment, one of the most striking findings to date to support [gene-environment] interaction,” researchers noted in the editorial.

According to the behavioral susceptibility theory, poorer appetite regulation and overeating, even in genetically predisposed subjects, is more likely to be expressed when a child is exposed to higher-risk environments.

“It is feasible that a home environment with multiple food cues triggers appetitive and reward-related pathways, which prompt increased food intake and, subsequently, weight gain,” investigators said.

Other theories involving the interplay of motivation, reward, and self-regulation may also improve our understanding of how the genetics of childhood obesity work.

The findings of this study shed light onto the mechanisms underlying obesity and offer some hope to families and doctors regarding what can be done to prevent obesity in children. Changing home lifestyle habits and promoting healthy eating and activity can partially counterbalance these children’s genetic susceptibilities and prevent them from gaining weight.

In the future, other aspects of the home environment may be explored; for example, the degree of cognitive stimulation — children raised with fewer stimuli (games, books, and activities) appear to be more likely to become obese.

Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she focused her research on molecular biology, epigenetics and infectious diseases.
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Ana is a molecular biologist enthusiastic about innovation and communication. In her role as a science writer she wishes to bring the advances in medical science and technology closer to the public, particularly to those most in need of them. Ana holds a PhD in Biomedical Sciences from the University of Lisbon, Portugal, where she focused her research on molecular biology, epigenetics and infectious diseases.
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