American Journal of Clinical Nutrition, Vol. 70, No. 2, 300-301,
August 1999
© 1999 American Society for Clinical Nutrition
Reply to PP García Luna et al
Steven Grinspoon
Massachusetts General Hospital Neuroendocrine Unit 55 Fruit Street, BUL 457B Boston, MA 02114
Dear Sir:
In our recent article, "Determinants of Increased Energy Expenditure in HIV-Infected Women," we showed significantly increased resting energy expenditure (REE) in ambulatory, HIV-infected women (1). REE was, in fact, 119% of that predicted by the Harris-Benedict equation, which agrees with the results of many previous studies showing increased energy expenditure in this population (2–4). In the patients studied, we found no correlation between REE and viral burden. In their accompanying editorial, Kotler and Heymsfield (5) noted that the results from our study are in contrast with those of Mulligan et al (6) obtained in 36 HIV-positive men, in whom REE was also significantly increased to 112% of that predicted by the Harris-Benedict equation. In the patients reported on by Mulligan et al, a significant positive correlation between REE, expressed per kilogram lean body mass, and viral load was noted. Furthermore, Kotler and Heymsfield suggested that a potential relation between REE and viral load might have been noted if our data had been log-transformed or if the patient population had been larger. However, no such positive relation was found even when the data were log-transformed (Figure 1
). In contrast, our data suggested an inverse correlation between REE and viral load.
Similarly, Suttmann et al (7) did not find a consistent relation between REE and immune function as measured by CD4 cell count in 60 HIV-infected patients (primarily men). In the accompanying letter, García Luna et al (8) also reported on the relation between REE and viral load. In 85 HIV-infected patients, no significant relation was found between REE and viral load and the overall r value for the comparison was negative. However, the data from García Luna et al are not broken down by sex, which would be useful, considering that the data from Mulligan et al were collected in men in contrast with our data in women.
The mechanism of increased REE in HIV-infected patients remains unknown and may relate to cytokine abnormalities or other factors (2). If REE were positively associated with viral load, it might be hypothesized, as suggested by Mulligan et al, that increased energy expenditure is a direct result of progressive HIV infection (6). As a corollary, control of HIV replication might result in reduced energy expenditure. Although this hypothesis remains an interesting one, we still must determine whether there is a relation between REE and viral load, and if so, whether there are sex-specific differences between HIV-infected men and women with respect to this relation. Further research is needed to better define the relation, if any, between REE and viral load. Useful data might be obtained from longitudinal studies in patients receiving potent antiviral agents, in whom REE could be assessed before and after therapy.
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