Does weight gain lead to weight loss?
Department of Psychology, Bishop's University, Lennoxville, QC, Canada, J1M 1Z7
e-mail: sblack{at}ubishops.ca
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Introduction |
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This is a remarkable claim with important theoretical and practical
implications. Indeed, the finding was cited by Shanas et al.
(2002) as a reason for not
implanting transmitters in spiny mice. Its importance did not escape the
notice of Nature Science Update, which featured the research under
the headline `Weight gain causes weight loss'
(Whitfield, 2001
).
Unfortunately, there is reason to question whether the phenomenon is real.
Mice were assigned to groups by matching on body weight rather than by randomization, the `gold standard' of experimentation. While this had the desired effect of eliminating body weight variability, it also created groups with significant pre-operative differences in food intake, a critical variable in this experiment. These pre-experimental differences compromise their post-experimental comparisons.
The authors' statistical analysis is a second cause for concern. They used
the NewmanKeuls procedure, a controversial test that does not control
the family-wise error rate (Curran-Everett,
2000). Inspection of the standard error bars on their figures
suggests that many of their comparisons were not significant as claimed. I
confirmed this by measuring the error bars and using the data to calculate
two-tailed t-tests. Most were not significant.
The data presented in their fig. 2 on changes in body weight after implantation are critical to their conclusions. First, I note that the data on the body weights of the mice plus their implant weights duplicate the data on true body weights, which alone provide meaningful data. Their fig. 2C presents this information as a function of implant weights. My analysis indicates that none of these comparisons is significant. For fig. 2D, which reports decreases in true body weight from pre-operative body weight, my analysis confirms that the decrease in body weight for the 2 g implanted group was significantly greater than for either of the two control groups. However, the 3 g implanted group did not differ significantly from any group. Consequently, these data do not support the claim that the weight loss was "proportional to the mass of the implant" (p. 1729).
Changes in food intake were also investigated, and "a clear trend for a reduction in food intake with increased implant mass" (p. 1732) was reported. Yet this claim is unsupported by statistical evidence. Moreover, while I confirm that the intake of the 3 g group was significantly lower than that of the sham control group, it did not differ significantly from the implant control group. Thus, the evidence for a proportionate decline in food intake as a function of increasing implant weight is unconvincing.
Following the experimental phase, the implants were removed from half the mice in each group and all groups were monitored for an additional seven weeks. These data, reported separately for each implant weight condition, are also problematic. The data are presented as changes in body weight from pre-operative body weight. Only the data that give the true body weights of these mice minus their implant weights are meaningful. Except for a brief period, the true body weights of those still carrying implants did not differ from those in which the implants had been removed, both maintaining true body weights approximately 1 g below their pre-operative weights. There was no proportionate effect of implant weight. However, because data for the two control groups were not provided, the significance of this small decrease in weight compared with pre-operative weight five or more weeks earlier cannot be evaluated. Thus, it cannot be concluded that the decrease in weight was caused by the prior experience of carrying an implant weight.
There is also an anomalous result. The weight of the groups with implants removed showed a transient increase that peaked on day 3 after implant removal. This represented a return to pre-operative body weight for the 1 g and 2 g groups. More remarkably, for the 3 g group, it represented an increase of almost 10% above pre-operative weight. This is an unusual response that the authors fail to directly note. Instead, they discuss the transient increase only in relation to the body weights of the mice including their implant weights, which obscures this puzzling result.
Overall, I commend the authors for an original and intriguing hypothesis. Unfortunately, their study failed to randomize subjects to groups, used questionable statistical analysis, failed to provide data for control groups for comparisons after the implants were removed, and reported an anomalous result. Consequently, the only reasonable answer to the question `does weight gain lead to weight loss?' is that we cannot yet claim that it does.
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Acknowledgments |
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References |
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Adams, C. S., Korytko, A. I. and Blank, J. L.
(2001). A novel mechanism of body mass regulation. J.
Exp. Biol. 204,1729
-1734.
Curran-Everett, D. (2000). Multiple
comparisons: philosophies and illustrations. Am. J. Physiol. Reg.
Integ. Comp. Physiol. 279,R1
-R8.
Shanas, U., Afik, D., Scantlebury, M. and Haim, A. (2002). The effects of season and dietary salt content on body temperature daily rhythms of common spiny mice from different micro-habitats. Comp. Biochem. Physiol. A 132,287 -295.
Whitfield, J. (2001). Weight gain causes weight loss. Nature Science Update 2 May 2001, http://www.nature.com/nsu/010503/010503-5.html.
Response to `Does weight gain lead to weight loss?'
1 Department of Orthopaedic Surgery, Thomas Jefferson University, Philadelphia,
PA 19107, USA
2 Department of Biological Sciences, Kent State University, Kent, OH 44242,
USA
* Author for correspondence (e-mail: christopher.adams{at}mail.tju.edu)
Accepted 20 March 2003
We were glad to learn that our study `A novel mechanism of body weight
regulation' (Adams et al.,
2001) was of interest to Dr Black and we thank him for his
creativity in re-interpreting our data
(Black, 2003
). The methods he
used for this re-interpretation, while imaginative, are incorrect inasmuch
as they are inappropriate to our experimental system. Black states four
subjects of concern that invalidate our claims. These are: (1) failure to
randomize; (2) questionable statistical analysis; (3) failure to provide
controls for fig. 4; and (4) an `anomalous result'.
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1. Failure to randomize |
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2. Questionable statistical analysis |
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To return to Curran-Everett and his criticism of the
StudentNewmanKeuls procedure, underestimation of error caused by
repeated measurements is a serious concern. In addition to the
StudentNewmanKeuls test, the least significant difference (LSD)
test also fails to control the probability of making a type I error.
Furthermore, another multiple comparison procedure, the Bonferroni inequality
test, is flawed in the other direction in that it may, in fact, fail to detect
actual differences. As reported by Curran-Everett
(2000), these three test are
the three most commonly used multiple comparison tests in journals published
by the American Physiological Society. To confirm that the results we
presented in the original paper are significant, we have returned to our
original data and reanalyzed it using a more conservative Tukey multiple
comparison procedure in place of the StudentNewmanKeuls test. We
found only two small differences in what the tests determined were
significant. These are both shown in Fig.
1. Unlike the StudentNewmanKeuls test, the Tukey
test did not determine significant differences between the sham control or the
implant control groups and the 2 g implant group for food intake
(fig. 1B in our original
paper). Therefore, despite Black's concerns regarding pre-operative food
intake, a more conservative post-hoc test actually shows
fewer pre-operative differences. The second change was seen in
fig. 2C of the original paper.
The Tukey test did not recognize a significant difference between the sham
control and the implant control. There were no other differences between the
results of the two tests. The differences that we did see do not alter our
interpretation of the data or the conclusions that are presented in the
paper.
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3. Failure to provide data for control groups for fig. 4 |
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4. An `anomalous result' |
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References |
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Adams, C. S., Korytko, A. I. and Blank, J. L.
(2001). A novel mechanism of body mass regulation. J.
Exp. Biol. 204,1729
-1734.
Black, S. L. (2003). Does weight gain lead to
weight loss? J. Exp. Biol.
206,2535
-2536.
Curran-Everett, D. (2000). Multiple
comparisons: philosophies and illustrations. Am. J. Physiol. Reg.
Integ. Comp. Physiol. 279,R1
-R8.