"Eating fried food is more likely to make you fat if you have 'obesity genes'," The Independent reports after a study in the BMJ suggested that those with a genetic predisposition towards obesity should avoid fried food.
The news is based on a US study that analysed interactions between fried food consumption and genetic risk factors associated with obesity (specifically, 32 known "genetic variants") in more than 37,000 men and women from three large US trials.
In particular, the researchers wanted to see if those people with the highest "genetic obesity risk profile" were more likely to put on weight if they consumed lots of fried food.
Participants in the studies were asked how often they consumed fried foods at home and away from home. Their weight and height was measured repeatedly for between three and 14 years.
The results showed that eating fried food more than four times a week had twice as big an effect on body mass index (BMI) for those with the highest genetic risk score compared with those with the lowest score.
Overall, this study provides some evidence of an association between fried food consumption and increased body fat based on genetic risk.
However, as all of the participants in the study were US-based health professionals, the findings may not apply to the population at large.
Another practical limitation is that unless you are willing to stump up for expensive genetic testing, it is usually unclear whether you are a "fat gene" carrier.
If you are worried about your weight, grilled food is normally the leaner alternative. For more information, visit the NHS Choices weight loss plan.
Where did the story come from?
The study was carried out by researchers from the Harvard School of Public Health and Harvard Medical School in the US, among other US institutions. It was funded by grants from the National Institutes of Health, with additional support from Merck Research Laboratories for genotyping.
The Mail Online and The Independent accurately reported the findings of the study. However, neither news outlet raises the point that aside from paying for testing – which, at the time of writing, is around £300 – it is difficult to tell whether an individual has one of the 32 known genetic variants for obesity.
Obesity does run in families, but can also be caused by a person's environment, rather than their genetics.
What kind of research was this?
This was a prospective cohort study. The study looked at the interaction between the frequency of eating fried food and a genetic risk score based on established genetic variants associated with BMI. The participants in the study were a group of US male and female health professionals.
A prospective study:
- asks a specific study question (usually about how a particular exposure affects an outcome)
- recruits appropriate participants
- looks at the exposures
- measures outcomes of interest in these people over the following months or years
Results from prospective studies are usually considered more robust than retrospective studies.
Retrospective studies either use data collected in the past for another purpose, or ask participants to remember what has happened to them in the past. This makes them prone to recall bias.
What did the research involve?
Researchers analysed data from three large US trials:
- 9,623 healthy female registered nurses from the Nurses' Health Study
- 6,379 healthy male health professionals from the Health Professionals Follow-up Study
- 21,421 healthy female health professionals from the Women's Genome Health Study
They used the first two trials to assess for interactions, and further analysis from the third, larger trial was used to see if their findings were replicated among this group.
The age of participants across the three studies ranged from 30 to older than 45 years.
Validated food frequency questionnaires were used in the three studies to assess fried food consumption at the start. Two studies continued to carry out the questionnaires at four-year intervals thereafter.
Participants were asked how often they consumed fried foods at home and away from home. The authors of the current study state they did not ask about the specific frying method, but report that most fried foods in the US are deep fried.
Three categories of fried food consumption were identified:
- less than once a week
- one to three times a week
- four or more times a week
The main outcome of interest was BMI, which was measured repeatedly over the follow-up period. Height and weight were assessed at the start of the three trials, and weight was requested at each follow-up questionnaire.
Self-reported weight was reported to be highly correlated with measured weight in a validation analysis. Lifestyle information such as smoking and physical activity was also collected.
The genetic risk score was based on 32 known genetic variants associated with BMI and obesity. Genetic risk scores ranged from 0 to 64, and those with a higher score had a higher BMI.
The researchers then examined the association between fried food consumption and BMI according to thirds of genetic risk score (highest third, middle third, and lowest third).
They report that they accounted for possible confounding factors from age-related weight change by only using follow-up data up to 1988. This allowed for three to four repeated measures of BMI in two of the studies.
What were the basic results?
The researchers found consistent significant interactions between fried food consumption and genetic risk scores on BMI in all three studies.
Among participants in the highest third of the genetic risk score, the differences in BMI between individuals who consumed fried foods four or more times a week and those who consumed fried foods less than once a week were 1.0 kg/m2 in women and 0.7 kg/m2 in men.
The corresponding score differences in the lowest third of the genetic risk score were 0.5 kg/m2 in women and 0.4 kg/m2 in men.
This shows that the genetic association with increased BMI was strengthened with higher consumption of fried foods. Or, in layman's terms, those with "fat genes" appeared to be more vulnerable to the fattening effects of fried foods.
The researchers also found significant interactions for fried food consumed both at home and away from home in one of the studies (9,623 healthy female registered nurses), and these interactions were replicated in a larger study (21,421 healthy female health professionals).
This means that significant interactions were found irrespective of eating fried food at home or out of the home. Similar interactions were observed in another study (6,379 healthy male health professionals), but these were non-significant.
Another finding was that variants in or near genes "highly expressed" or known to act in the central nervous system showed significant interactions with fried food consumption, with the "fat mass and obesity-associated variant" showing the strongest result.
How did the researchers interpret the results?
The authors concluded that consistent results from three studies indicate that the association between fried food consumption and adiposity (body fat) might vary according to differences in genetic predisposition and, vice versa, the genetic influences on adiposity might be modified by fried food consumption.
In discussing the research, assistant professor Lu Qi from the Harvard School of Public Health states that, "Our findings emphasise the importance of reducing fried food consumption in the prevention of obesity, particularly in individuals genetically predisposed to adiposity".
In an editorial commenting on the research, also published in the BMJ, the two authors from Imperial College London report: "This work provides formal proof of interaction between a combined genetic risk score and environment in obesity". However, they said the results "are unlikely to influence public health advice, since most of us should be eating fried food more sparingly anyway".
Overall, this study provides some evidence of interactions between fried food consumption and adiposity based on genetic risk.
The authors rightly acknowledge the strengths of the study, such as:
- the inclusion of large cohort studies with long-term follow-up
- multiple measures of fried food consumption and BMI
- the use of a genetic risk score that combined genetic information of 32 variants known to be associated with BMI
Several of the study's limitations as reported by the authors include:
- a causal relationship between fried foods, genetic variants and adiposity cannot be proven by an observational study such as this one
- results may have been affected by other unmeasured or unknown factors, despite attempting to carefully adjust the results for several diet and lifestyle factors
- specific information about foods the participants consumed, such as the type of oil used for frying or the type of frying performed, were not collected in this study – this may have limited the depth of analyses in the study
- similarly, no information was provided on the amount of fried food consumed on each occasion
- errors in measuring fried food consumption are possible because of the self-reporting nature of the food frequency questionnaire, although the researchers do report the questionnaire has been well validated
- differences in gender were not tested – the researchers report this was because each of the three studies had only male or female participants
Further limitations of the study are that as all participants were health professionals in the US, findings may not be generalisable to the general population. This is especially true because, as health professionals, these people may have been better informed about taking care of their health.
Another consideration is that methods for cooking fried food may be different in the US compared with techniques used in the UK. The authors report that most fried foods in the US are deep fried, and this may not be in the case in the UK.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
The Independent, 19 March 2014
Mail Online, 19 March 2014
Links to the science
BMJ. Published online March 19 2014