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Are five meals a day key to tackling teen obesity?

“The cure for teen obesity? Eating five times a day,” is the advice on the Mail Online website.

It reports on a study that looked at how frequently a large number of teenagers ate their daily meals, and whether this might affect the impact of genetic risk factors for being obese. A number of genetic variants have been identified as being associated with an increased risk of an individual becoming obese.

The researchers found that in adolescents who ate five meals a day (three standard meals plus two snacks), genetic risk factors seemed to have less of an effect on body mass index (BMI).

However, the main limitation of this study is that meal frequency was assessed at the same time as BMI, so researchers can’t say for certain whether meal frequency was affecting BMI or vice versa. They also didn’t have information about what the participants ate, so couldn’t see how the number of calories consumed compared between those eating five meals a day and those who did not.

Although this study by itself is not conclusive, there is a growing interest in how our eating patterns, and not just what we eat, is linked to our risk of being overweight. It is hoped that a better understanding of these links will help people know how best to maintain a healthy weight.

Where did the story come from?

The study was carried out by researchers from the University of Eastern Finland and other research centres in Finland, the UK and France. It was funded by the Academy of Finland and the Nordic Centre of Excellence on SYSDIET (systems biology in controlled dietary interventions and cohort studies).

The study was published in the peer-reviewed open access journal PLoS One, which can be read online or downloaded for free.

The Mail Online’s headline uses the word “cure”, a word that needs to be used with more caution. It is unlikely that regular mealtimes on their own are a “cure” for obesity, and this is not what the study itself suggests.

The Mail also refers to the genetic risk factor as “eight gene mutations that cause obesity”, which is a bit of an oversimplification. The genetic variants in question are common among the population and don’t “cause” obesity: they are in fact associated with an increased chance of a person being overweight.

Both genetic and environmental factors (diet and physical activity) play a role in a person’s weight. Carrying these genetic variants may mean a person is more likely to gain weight, but they don’t guarantee that they will be overweight or obese, or make it impossible to lose weight.

The Mail also reports on other findings from this ongoing study, such as the impact of maternal obesity in pregnancy on child obesity. These findings were not part of the study in the PLoS publication being covered. The accuracy of the reporting of these claims has not been reported here.

What kind of research was this?

This was cross-sectional analysis that looked at the relationship between meal frequency and BMI in adolescents with and without genetic risk factors for obesity.

The causes of obesity are complex, and include genetic and environmental factors. Genome wide analyses have identified many common genetic variants linked to an increased risk of obesity. These genetic variants do not guarantee that a person will be overweight; instead, people who carry them have a higher risk of being overweight. Some studies have suggested that patterns of eating – such as meal frequency – also have an effect.

The researchers found in a previous study that 16-year-olds who ate five meals a day were less likely to be overweight or obese. In the current study, they wanted to see if meal frequency might “modify” the effect of genetic risk factors in adolescents. That is, whether adolescents genetically predisposed to be overweight might be less likely to have a higher BMI if they ate five meals a day rather than fewer meals.

What did the research involve?

The researchers assessed mealtime habits, BMI and genetic risk factors for obesity in 4,669 Finnish teenagers. They looked at how these factors were inter-related, particularly how meal frequency was related to BMI in teenagers with or without a genetic predisposition to becoming overweight.

The study analysed adolescents taking part in the prospective Northern Finland Birth Cohort 1986, an ongoing cohort study. This study recruited 9,432 infants born in the two northernmost provinces of Finland to women with expected delivery dates between July 1, 1985 and June 30, 1986. This represented 99% of the eligible births in the region. The participants have been followed up since the pregnancy.

The current study used data collected at one point in time when the children were 16 years old. At this age, they had a clinical examination where blood was collected for DNA extraction, and their height and weight was measured to allow their BMI to be calculated. They also filled in a postal questionnaire about health behaviours, including one question about meal frequency. This question asked if they usually ate the following five meals on a weekday:

  • breakfast
  • lunch
  • snack
  • dinner
  • evening snack

The researchers checked whether the participants carried eight genetic variants associated with an increased risk of obesity. Each participant had their own “genetic risk score”, which was the sum of all the genetic risk variants they carried. The current study only included participants who had complete data on all of the factors being analysed.

The researchers then analysed whether meal frequency and genetic risk score were associated with BMI. They also looked at whether meal frequency impacted the relationship between genetic risk score and BMI. In these analyses, they took into account the participants’ gender and stage of puberty.

What were the basic results?

The average BMI among the study participants was 21.2 kg/m2. The researchers found that adolescents with a high genetic risk score (eight risk variants or more) had an average BMI 0.7 kg/m2 higher than those with a low genetic risk score (fewer than eight risk variants). Adolescents who usually ate five meals a day had an average BMI 0.9 kg/m2 lower than those who had fewer meals. Genetic risk score and meal patterns were not related.

When the researchers looked at individuals with different meal patterns separately, they found that the effect of the genetic risk factors was less among those who ate five meals a day. In adolescents who ate five meals a day, each additional genetic risk variant was associated with a 0.15 kg/m2 increase in BMI, compared with a 0.27 kg/m2 increase among those who did not eat five meals a day.

For an adolescent who was 170cm tall, this would mean each additional genetic risk variant was associated with a 0.43kg increase in weight for those who did eat five meals a day, compared with a 0.78kg increase among those who did not eat five meals a day.

Among those who ate five meals a day, the difference in BMI between those with high genetic risk scores and low scores was 0.32 kg/m2, while in those who didn’t the difference was greater (0.90 kg/m2).

How did the researchers interpret the results?

The researchers concluded that having a regular five meals a day pattern reduced the impact of genetic risk factors on BMI in adolescents. They suggest that promoting regular eating patterns could be an effective obesity prevention strategy.

Conclusion

This study has suggested that having regular meals is associated with a reduced impact of genetic risk factors for being overweight in adolescents. The study was part of an ongoing cohort study, which benefits from the fact that it included a high proportion of the eligible population, its prospective data collection, and standard measurement of BMI.

There are two main limitations of the current study. Although it was part of a cohort study, the analyses only looked at data collected at one point in time, when the children were 16 years old. Their genetic risk factors would have been present from conception and therefore would have preceded their current BMI.

However, their reported meal patterns may not have preceded their current BMIs, and there may be some “reverse causality” at play. This means that the adolescents may be adapting their meal pattern as a result of their BMI and not vice versa, so if they think they are overweight, they may try to restrict their meals.

The second main limitation is that only a small amount of information was collected on meals. Only one question was asked about meal frequency, and this question had not been tested for how well it matched data collected in food diaries, for example. Also, no data was collected on what the adolescents ate, so this could not be taken into account in the analyses. It is not clear how the number of calories or types of foods those eating five meals a day were eating compared with those who did not have this number of meals a day.

It is also worth noting that BMIs are interpreted differently for children and young people aged under 18 than for adults. It was not clear if any of the adolescents in the current study would have been considered overweight or obese.

This study illustrates a growing interest in how we eat and what we eat, as well as the relationship between genetic and environmental risk factors for obesity.

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