Gender difference in interactions between MAOA promoter uVNTR polymorphism and negative familial stressors on body mass index among Chinese adolescents
What is already known about this subject
- Initial evidence from recent studies indicated a relationship between the high-activity MAOA uVNTR polymorphism and lower risk of obesity even though findings were varied across populations, and hence replication studies with population-based samples are clearly warranted.
What this study adds
- Our findings confirmed the genetic effects of MAOA uVNTR polymorphism on body mass index in a Chinese adolescent population.
- This study demonstrated a significant gene–environment interaction with negative familial stressors in girls only, which provides a new insight on the causes of obesity, and thus, potential avenues of prevention.
Monoamine oxidase A (MAOA) modulates metabolism of serotonin and dopamine metabolism, neurotransmitters involved in regulation of appetite and food intake. The gene coding for MAOA contains a 30-bp tandem repeat (uVNTR) polymorphism in its promoter region that has been previously identified to be associated with obesity with mixed findings in the literature. Our goals were to replicate the population effects of this functional polymorphism on obesity risk, and to further explore gender differences and interaction effects with negative stressors.
Analyses were conducted with data on genotypes, measured weight and height, and self-reported behavioural characteristics among 1101 Chinese adolescents 11–15 years old living in Wuhan, China.
Girls with the high-activity allele had significantly lower body mass index (BMI; β = −0.25 ± 0.98, P = 0.011) compared to those with the low activity allele. Experience of negative familial stressors (e.g., death or illness of family members, hit or scolded by parents and increased quarrelling with parents, parents argued frequently) significantly weakened this protective genetic effect on BMI (P for interaction = 0.043). Stratified analyses showed a significant protective genetic effect on BMI only within the stratum of low stress level (β = −0.44 ± 0.14, P = 0.002). No similar effect was observed among boys.
Our findings confirm the genetic effects of MAOA uVNTR polymorphism on BMI in a Chinese adolescent population and suggest potential genetic interactions with negative familial stressors.