Obesity, smoking, and frontal brain dysfunction

Lance Bauer, Danielle Dick, Laura Bierut, Kathleen Bucholz, Howard Edenberg, Samuel Kuperman, John Kramer, John Nurnberger, Sean O'Connor, John Rice, John Rohrbaugh, Marc Schuckit, Jay Tischfield, Bernice Porjesz, Victor Hesselbrock

Research output: Contribution to journalArticlepeer-review

13 Scopus citations


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.

Original languageEnglish
Pages (from-to)391-400
Number of pages10
JournalAmerican Journal on Addictions
Issue number5
StatePublished - Sep 2010


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