| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Letters to the Editor |
Center for Human Nutrition, University of Colorado, Denver, CO, Weill Medical College of Cornell University, The Comprehensive Weight Control Program, New York, NY
Dear Sir:
McCarthy makes several interesting points about our study of the lipase inhibitor orlistat for the prevention of weight regain. Some of these issues were discussed previously in a letter by McCarthy (1) to the Editor of The Lancet and in the response to McCarthy by Sjöström et al (2).
We agree with McCarthy's comments that dietary fat specifically is an appropriate target in obesity management, in addition to total energy intake, and that the gut may be an important target of medical therapy that may be attacked with virtually no systemic side effects. Although we did not obtain any data regarding satiety in our study, the fact that self-reported dietary intakes were fairly stable over 1 y and were not significantly different between the orlistat and placebo groups supports McCarthy's suggestion that the brain does not appear to compensate for the 30% malabsorption of dietary fat produced by orlistat. However, we would like to point out that Figure 3 in our paper (3) does not indicate that orlistat treatment reduced the subjects' fat intake 5-fold more than placebo, as he states in his letter. Indeed, according to self-reported intakes, the 2 treatment groups consumed similar amounts of dietary fat and the lesser weight regain in the orlistat group was attributable to the mechanism of action of the drug, which effectively converted a 30%-fat diet to a 24%-fat diet by rendering one-third of the fat energy unavailable for storage or utilization. Thus, the difference between the treatment groups was attributable to the pharmacologic effect of orlistat on the absorption of dietary fat rather than to an aversive effect that drove the dietary fat intake of the orlistat-treated patients below that of the placebo group. However, it is possible that avoidance of gastrointestinal side effects could play a role in controlling consumption of dietary fat in excess of the recommended 30%.
We agree that weight loss without the use of medication would be optimal. In clinical practice, however, some patients cannot achieve and most patients cannot sustain long-term weight loss. Orlistat is intended for use as an adjunct to a program of diet and exercise. It is not meant to take the place of a program of lifestyle and behavioral changes. Whereas the difference in weight loss maintained between the placebo and orlistat groups appears modest, previously published studies of orlistat use showed that small weight losses can be clinically significant in preventing relapse of obesity-related complications (4, 5). Furthermore, categorical analysis of the percentage of patients who lost >10% of initial body weight with orlistat shows that, as with many drugs, some patients do extremely well, whereas others may not (5). In clinical practice, for example, we do not continue to give an antihypertensive agent that does not lower blood pressure; additional or alternative treatment options are considered. We suspect the same will be true of antiobesity agents, including orlistat; patients who are successful will continue to use them, and those who are not may require additional counseling, dietary advice, or therapies. Last, although there is great value in identifying factors related to successful weight management, one should cautiously compare the 30-kg weight loss sustained over 5 y in the cohort of patients enrolled in the National Weight Control Registry (6) with other obesity treatments because the former is a self-selected population whose experience may not be typical of that of most obese adults.
Obesity is a disorder of overnutrition. There are no data that we are aware of to support the suggestion that consuming a diet containing 30% fat coupled with lipase inhibition to block the absorption of one-third of dietary fat energy is different from simply consuming a diet that is 
20–25% fat with respect to the micronutrient content or fat-soluble vitamin contents. Diets containing similar amounts of dietary fat have not been shown to produce micronutrient or vitamin deficiencies (7).
Finally, we concur with McCarthy that there is a need for further research regarding satiety. We also agree that there are many areas of future research that could potentially improve the long-term efficacy of obesity treatment, including the extent to which orlistat therapy may act as a deterrent to dietary fat consumption in some patients, interactions between dietary intake and exercise, and existing and future pharmacologic options.
REFERENCES
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
