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Reply to R Cooper and A Luke

Department of Family Medicine & Clinical Epidemiology University of Pittsburgh School of Medicine 3518 Fifth Avenue E-mail: kimm{at}pitt.edu

Dear Sir:

We appreciate the comments of Cooper and Luke in response to our recently published report (1). Although we welcome a lively debate in the interest of scientific inquiry, we are concerned that Cooper and Luke attribute to us conclusions that we did not actually draw. We agree that multiple hypothesis testing can be problematic. For this reason, we presented the estimated P value for all of our tests so that readers may draw their own conclusions from the data. Certainly, our sample size was small, and that is the reason all of our conclusions were expressed only as tantalizing clues. We stated, "This observation of racial differences in the UCP3 exon 5 gene effect is made more complex by the overall small sample size in the present study...." We also acknowledged that further study with a larger sample size is necessary.

As for the writers’ concern about the nature of the causal inference made, we noted in our report that the polymorphism in question is not a functional change and therefore cannot be causal. Our primary analysis considered only resting energy expenditure, not obesity. Our secondary (ie, exploratory) analysis examined adiposity, not obesity. Hence, we refute the assertion that we made a "causal inference" regarding obesity. Nowhere do we "conclude" that the UCP3 genotype is a "cause" of differential racial susceptibility to obesity. Any connection made with racial differences in obesity appears only in our speculative discussion at the end of a report in which no conclusions were drawn.

In any genetic study, the definition of phenotype is critical. In our analysis, the phenotype was resting energy expenditure, not obesity or body mass index. Cooper and Luke seem to suggest that this is not the "phenotype of interest." We strongly disagree, because we believe that attempts to understand differences in resting energy expenditure will lead to a better understanding of the metabolic aspect of the energy balance equation.

We agree with Cooper and Luke on the crucial role that lifestyle plays. In fact, our concluding statement is, "...the high prevalence of obesity in African American women in the United States today may be the result of their contemporary lifestyle of relatively high energy intake and physical inactivity in the presence of an underlying genetic propensity for efficient energy conservation."

Finally, Cooper and Luke are mistaken in their assertion that we have longitudinal data on resting energy expenditure and weight change. We have data on resting energy expenditure at only one time point, when the study subjects were aged 18–21 y.

We hope that this response fully addresses and helps clarify some of the issues raised by Cooper and Luke.

REFERENCE

1. Kimm SYS, Glynn NW, Aston CE, et al. Racial differences in the relation between uncoupling protein genes and resting energy expenditure. Am J Clin Nutr 2002;75:714–9.[Abstract/Free Full Text]

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