TY - JOUR
T1 - Obesity, smoking, and frontal brain dysfunction
AU - Bauer, Lance
AU - Dick, Danielle
AU - Bierut, Laura
AU - Bucholz, Kathleen
AU - Edenberg, Howard
AU - Kuperman, Samuel
AU - Kramer, John
AU - Nurnberger, John
AU - O'Connor, Sean
AU - Rice, John
AU - Rohrbaugh, John
AU - Schuckit, Marc
AU - Tischfield, Jay
AU - Porjesz, Bernice
AU - Hesselbrock, Victor
PY - 2010/9
Y1 - 2010/9
N2 - Obesity, smoking, and conduct problems have all been associated with decrements in brain function. However, their additive and interactive effects have rarely been examined. To address the deficiency, we studied P300a and P300b electroencephalographic potentials in 218 women grouped by the presence versus absence of: (1) a BMI ≥ 30 kgm2; (2) recent smoking; and (3) ≥ 2 childhood conduct problems. Analyses revealed smaller P300a and P300b amplitudes over the posterior scalp among recent smokers versus nonsmokers. No corresponding group differences were found in P300 latencies or frontal scalp amplitudes. The most interesting analysis result was an interaction between conduct problems and obesity limited to the frontally generated P300a component: its latency was significantly greater in women with both attributes than in those with either or neither attribute. An exploratory ANOVA, substituting the genotype of a GABRA2 SNP for conduct problems, also demonstrated an interaction with obesity affecting P300a latency. It is hypothesized that conduct problems, and a conduct-problem-associated GABRA2 genotype, decrease the age-of-onset andor increase the lifetime duration of obesity. As a result, they may potentiate the adverse effects of obesity on frontal white matter and thereby increase P300a latency. Smoking may affect brain function by a different mechanism to reduce posterior scalp P300a and P300b amplitudes while preserving frontal scalp P300a latency and amplitude.
AB - Obesity, smoking, and conduct problems have all been associated with decrements in brain function. However, their additive and interactive effects have rarely been examined. To address the deficiency, we studied P300a and P300b electroencephalographic potentials in 218 women grouped by the presence versus absence of: (1) a BMI ≥ 30 kgm2; (2) recent smoking; and (3) ≥ 2 childhood conduct problems. Analyses revealed smaller P300a and P300b amplitudes over the posterior scalp among recent smokers versus nonsmokers. No corresponding group differences were found in P300 latencies or frontal scalp amplitudes. The most interesting analysis result was an interaction between conduct problems and obesity limited to the frontally generated P300a component: its latency was significantly greater in women with both attributes than in those with either or neither attribute. An exploratory ANOVA, substituting the genotype of a GABRA2 SNP for conduct problems, also demonstrated an interaction with obesity affecting P300a latency. It is hypothesized that conduct problems, and a conduct-problem-associated GABRA2 genotype, decrease the age-of-onset andor increase the lifetime duration of obesity. As a result, they may potentiate the adverse effects of obesity on frontal white matter and thereby increase P300a latency. Smoking may affect brain function by a different mechanism to reduce posterior scalp P300a and P300b amplitudes while preserving frontal scalp P300a latency and amplitude.
UR - http://www.scopus.com/inward/record.url?scp=77955777928&partnerID=8YFLogxK
U2 - 10.1111/j.1521-0391.2010.00069.x
DO - 10.1111/j.1521-0391.2010.00069.x
M3 - Article
C2 - 20716301
AN - SCOPUS:77955777928
SN - 1055-0496
VL - 19
SP - 391
EP - 400
JO - American Journal on Addictions
JF - American Journal on Addictions
IS - 5
ER -