OBJECTIVE: The aim of this work is to understand whether shared genetic influences can explain the association between obesity and cognitive performance, including slower and more variable reaction times (RTs) and worse response inhibition. METHODS: RT on a four-choice RT task and the go/no-go task, and commission errors on the go/no-go task for 1,312 twins ages 7-10 years were measured. BMI was measured at 9-12 years. Biometric twin models were run to give an estimate of the genetic correlation (rG ) between body mass index (BMI) and three cognitive measures: mean RT (MRT), RT variability (RTV; the standard deviation of RTs), and commission errors (a measure of response inhibition). RESULTS: Genetic correlations indicated that 20%-30% of the genes underlying BMI were shared with both RT measures. However, only small phenotypic correlations between MRT and RTV with later BMI (rPh = ∼0.1) were observed. Commission errors were unassociated with later BMI (rPh = -0.03, ns). CONCLUSIONS: Our results are the first to demonstrate significant shared genetic effects between RT performance and BMI. Our findings add biological support to the notion that obesity is associated with slower and more variable RTs. However, our results also emphasize the small nature of the association, which may explain previous negative findings.
OBJECTIVE: The aim of this work is to understand whether shared genetic influences can explain the association between obesity and cognitive performance, including slower and more variable reaction times (RTs) and worse response inhibition. METHODS: RT on a four-choice RT task and the go/no-go task, and commission errors on the go/no-go task for 1,312 twins ages 7-10 years were measured. BMI was measured at 9-12 years. Biometric twin models were run to give an estimate of the genetic correlation (rG ) between body mass index (BMI) and three cognitive measures: mean RT (MRT), RT variability (RTV; the standard deviation of RTs), and commission errors (a measure of response inhibition). RESULTS: Genetic correlations indicated that 20%-30% of the genes underlying BMI were shared with both RT measures. However, only small phenotypic correlations between MRT and RTV with later BMI (rPh = ∼0.1) were observed. Commission errors were unassociated with later BMI (rPh = -0.03, ns). CONCLUSIONS: Our results are the first to demonstrate significant shared genetic effects between RT performance and BMI. Our findings add biological support to the notion that obesity is associated with slower and more variable RTs. However, our results also emphasize the small nature of the association, which may explain previous negative findings.
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