Investigators in Scotland found that food cravings may be determined by a genetic mutation associated with obesity.  

by Peggy Peck, Executive Editor, MedPage Today

DUNDEE, Scotland, Dec. 10 — The likelihood of craving a couple of calorie-laden burgers and a cupcake or two instead of consuming a simple rice cake may be determined by a genetic mutation associated with obesity, found investigators here.

The effect of the mutation in a subset of children appears to involve control of both the amount of food consumed and the desire to consume dense, high calorie foods, researchers reported in the Dec. 11 issue of the New England Journal of Medicine.

Children who carried a variant of rs9939609, a fat mass and obesity-associated (FTO) gene, consumed more food at test meals than controls (P=0.006) and were also more likely to choose a burger over a rice cake, according to Colin N.A. Palmer, Ph.D., of the University of Dundee’s Biomedical Research Institute at Ninewells Hospital and Medical School, and colleagues.

And while total and resting energy expenditures were increased in children who were carriers of the A allele, resting energy expenditure was “identical to that predicted for the age and weight of the child, indicating that there is no defect in metabolic adaptation to obesity,” they wrote.

The findings emerged from a study of 2,726 Scots children ages four to 10 who had genotyping and height and weight measurement.

A sub-sample of 97 children who had the A allele variant of rs9939609 were also assessed for adiposity, energy expenditure, and food intake.

“In the total study group, the A allele of rs9939609 was associated with significantly increased weight (P =0.003) and BMI (P=0.003),” they wrote.

And in the subset of 97 children there were similar associations for weight (P=0.049) and BMI (P =0.03) and there was also an association with anthropometric skinfold values (P=0.03).

On the basis of the skinfold measurements, “children who carried the A allele had an estimated fat mass that was 1.78 kg greater than that of non-carriers (P=0.01) and an estimated lean mass that was less than 400 g greater than that of non-carriers ( P=0.46).

The authors said that their data “suggest that the [fat mass and obesity-associated] gene influences the ‘input’ side of the energy-balance equation,” a finding already reported in animal studies.

Thus the key to preventing obesity in people with this genotype, which occurred in 0.385% of the population studied, would be “moderate and controlled restriction of energy intake.”

In an editorial, Rudolph L. Leibel, M.D., of Columbia University in New York, wrote that the frequency of the rs9939609 A allele has been estimated as “0.45 in Europeans, 0.52 in West Africans, and 0.14 in Chinese.”

And even though the “locus accounts for only a small proportion of differences in BMI in the entire population, it plays a substantial role — in these people, in these environments — in conveying the risk of actually becoming overweight or obese.”

Although Dr. Leibel said it was too soon to consider genetic screening for obesity risk, but said the data from the school children in Scotland underscore the “important role the environment plays in enabling or resisting such susceptibility.”

Action Points 
————–

Explain to interested patients that this study suggested that a genetic variant controls both appetite and the types of food consumed.

Explain to interested patients that maintaining normal weight should be a goal regardless of age.

Explain to interested patients that current guidelines recommend a mix of diet and exercise for weight control.


The study was supported by a grant from the U.K. Biotechnology and Biological Sciences Research Council.
Dr. Palmer had no disclosures. Dr Leibel disclosed consulting fees fro Arisaph, Centocor, Genaera, ImClone, and Merck.

Published: December 10, 2008

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco  Earn 
 
Primary source: New England Journal of Medicine

Source reference:Cecil JE et al “An obesity-associated FTO gene variant and increased energy intake in children” N Eng J Med 2008: 359: 2558-66.

Additional source: New England Journal of Medicine

Source reference: Leibel R L “Energy in, energy out, and the effects of obesity-related genes” N Engl J Med 2008; 359: 2603-04.

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