Appetite disinhibition rather than hunger explains genetic effects on adult BMI trajectory.
International Journal of Obesity 2020 ; 45: 758-765.
Brunner EJ, Maruyama K, Shipley M, Cable N, Iso H, Hiyoshi A, Stallone D, Kumari M, Tabak A, Singh-Manoux A, Wilson J, Langenberg C, Wareham N, Boniface D, Hingorani A, Kivimaki M, and Llewellyn C
DOI : 10.1038/s41366-020-00735-9
PubMed ID : 33446837
PMCID : PMC8005371
URL : https://www.nature.com/articles/s41366-020-00735-9
The mediating role of eating behaviors in genetic susceptibility to weight gain during mid-adult life is not fully understood. This longitudinal study aims to help us understand contributions of genetic susceptibility and appetite to weight gain.
We followed the body-mass index (BMI) trajectories of 2464 adults from 45 to 65 years of age by measuring weight and height on four occasions at 5-year intervals. Genetic risk of obesity (gene risk score: GRS) was ascertained, comprising 92 BMI-associated single-nucleotide polymorphisms and split at a median (=high and low risk). At the baseline, the Eating Inventory was used to assess appetite-related traits of 'disinhibition', indicative of opportunistic eating or overeating and 'hunger' which is susceptibility to/ability to cope with the sensation of hunger. Roles of the GRS and two appetite-related scores for BMI trajectories were examined using a mixed model adjusted for the cohort effect and sex.
Disinhibition was associated with higher BMI (β = 2.96; 95% CI: 2.66-3.25 kg/m), and accounted for 34% of the genetically-linked BMI difference at age 45. Hunger was also associated with higher BMI (β = 1.20; 0.82-1.59 kg/m) during mid-life and slightly steeper weight gain, but did not attenuate the effect of disinhibition.
Appetite disinhibition is most likely to be a defining characteristic of genetic susceptibility to obesity. High levels of appetite disinhibition, rather than hunger, may underlie genetic vulnerability to obesogenic environments in two-thirds of the population of European ancestry.