Could a DNA test predict obesity risk in children?
“A DNA blood test can predict obesity levels in children as they grow up, scientists claim,” the Metro reports. The test, which is based on measuring “switches” in DNA, may help identify children who would benefit from early intervention.
This was a small study of 40 children who had their DNA analysed during early childhood. The test is based on a process called methylation. This is a chemical process that can influence the effects of genes on the body (gene expression), essentially “turning off” certain genes. Methylation can have both positive and negative effects.
The analysis did find an association between methylation at four sites in the DNA and increased body fat between the ages of nine and 14. But this study does not prove that the modifications directly caused the increased body fat.
It took into account the children’s age, sex, time of reaching puberty and an estimate of physical activity, but other important factors were not accounted for, including the children’s diets.
Read more advice about helping your child keep to a healthy weight.
Where did the story come from?
The study was carried out by researchers from the universities of Southampton, Plymouth and Exeter, and was funded by Bright Future Trust, BUPA Foundation, Kirby Laing Foundation, Peninsula Medical Foundation, the EarlyBird Diabetes Trust and the National Institute for Health Research.
It was published in the peer-reviewed medical journal, Diabetes.
The media has largely focused on the possibility that a blood test in young children could predict obesity in adolescence.
The study did find an association between certain genetic modifications and later obesity in a small sample of children.
However, it has not yet been determined how well any such test would perform in a larger sample of children. It is also not clear whether it would help prevent obesity in the children identified.
What kind of research was this?
This was a cohort study of children, following them from the age of five to 14 to see if certain genetic modifications could predict later levels of obesity.
The modifications being studied were not changes to the DNA sequence, but the presence of certain chemical modifications to the DNA (called methylation) that affect whether a gene is active or not. These chemical changes are part of the normal way that genes are controlled in the body.
This type of study design is appropriate for this type of question, as it followed the children over a long period of time and can show if there is a link.
In this type of study, researchers try to isolate the effect of one factor among the many that might be having an effect. But it is very difficult to account for all of these factors, especially for a condition as complex as obesity, which can be influenced by genetic, environmental and sociodemographic factors.
What did the research involve?
The researchers annually assessed 40 children over nine years to see if they could identify whether the status of a gene that is important for energy metabolism was associated with obesity.
They looked at the chemical modification (methylation) of various sites in the DNA before the children reached the age of five, then seeing whether this changed during childhood and if it could predict levels of obesity in later childhood.
The researchers looked at the methylation of part of peroxisomal proliferator-γ-co-activator-Iα (PCGIα), a gene that codes for a protein involved in energy metabolism. They examined seven specific sites in the DNA within this gene.
Previous studies have found that these seven sites have mostly been methylated in overweight adults with type 2 diabetes mellitus compared with adults of a normal weight. Methylation suppresses the activity of the gene.
The researchers recruited a random sample of 40 children (20 girls and 20 boys) in 2000-01 from a larger study called the EarlyBird study. Between the ages of five and 14, each year the children:
- had a blood test to measure insulin resistance and methylation at the seven sites in PCGIα
- had height and weight measurements taken to calculate body mass index (BMI)
- had a measurement of body composition (such as the amount of fat) using a technique called dual X-ray absorptiometry from the age of nine
- wore a motion monitor (accelerometer) for seven days so physical activity levels could be measured
- had height measurements taken to determine the age of reaching puberty
The researchers also measured the percentage of the sites that were methylated at each age. They then looked at whether there was an association between the percentage that were turned off at five years old and the child’s level of fat between the ages of nine and 14.
What were the basic results?
Results were available for 34 of the 40 children.
The level of methylation of the seven sites in PCGIα was relatively stable over the nine years of the study. At one site, for each 10% increase in the level of methylation at age five to seven years, body fat increased by 12.5% (95% confidence interval [CI] 4.7 to 20.3) between the ages of nine and 14.
Similar, but lower, levels of increased body fat (6.3 to 7.6%) were also found to be associated with methylation at three other sites.
There was no association between methylation of these four sites and sex, level of physical activity or time of reaching puberty. Age was only associated with methylation at one site.
There were no associations between the level of body fat and the level of methylation of the other three sites.
How did the researchers interpret the results?
The researchers concluded that measuring methylation of these sites in PCGIα in childhood may be useful in predicting cardio-metabolic disease risk (obesity-related diseases such as type 2 diabetes and heart disease).
This small cohort showed an association between chemical modification (methylation) of four sites in a gene (PCGIα) that codes for a protein involved in energy metabolism in young children, and increased body fat between the ages of nine and 14.
This study has found an association, but it cannot prove that methylation was directly responsible for increased body fat. For example, while the association was still there despite accounting for sex, age, estimated physical activity levels and puberty, other factors such as diet were not assessed.
A further limitation is that physical activity levels were measured for only seven days each year. This will give a rough indication of activity levels, but may not be an accurate representation of physical activity over the entire year.
The researchers themselves point out that the findings cannot rule out the possibility that the difference in the levels of fat in the children was because of calorie intake, another environmental factor or other genetic factors.
The study’s findings do not tell us how well a test based on these genetic modifications would perform at predicting body fat in a large sample of young children, not least because multiple genetic and environmental factors are likely to contribute to a child’s weight.
Even if a child is born with an increased vulnerability to obesity, it certainly does not mean that this is a fate set in stone.
The benefits of children staying active and eating a healthy diet have been well documented, and this study does not change the current advice.
If you are worried about your child’s weight, it is best to act now rather than ignore the problem. The longer this type of a problem is ignored, the more difficult it can become to treat.