What is adaptive thermogenesis
Though most studies did find increases in EE during overfeeding, these were mainly explained by the theoretical energy costs of weight gain and the maintenance of a larger body weight. Changes in EE above these obligatory costs are considered adaptive thermogenesis, but the magnitude is generally no more than a few percent and includes measurement errors, errors in assumptions made and small day-to-day differences in physical activity. In addition, results from different overfeeding studies are hard to pool as there are marked differences in macronutrient composition, measurement techniques and availability of data within the papers.
The latter causes comparison between studies using one measure i. Moreover, individual variation is lost using the mean values. This makes the existence of adaptive thermogenesis hard to prove. However, there are large differences in thermogenesis and weight gain between subjects, independent of body weight. In search for evidence for adaptive thermogenesis, it would therefore be interesting to define obesity-prone and obesity-resistant persons based on their response to overfeeding and in general it seems desirable to report individual data as well as group statistics.
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The effect of fat over-feeding on 24 h energy expenditure. Download references. You can also search for this author in PubMed Google Scholar. This article is published under license to BioMed Central Ltd. Reprints and Permissions. Joosen, A. Energy expenditure during overfeeding.
Nutr Metab Lond 3, 25 Metabolic slowing and reduced oxidative damage with sustained caloric restriction support the rate of living and oxidative damage theories of aging. Cell Metab. Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide. Sign In or Create an Account.
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Volume On adaptive thermogenesis: just another weight-loss tale? Faidon Magkos Faidon Magkos. Address correspondence to FM E-mail: fma nexs. Oxford Academic. Cite Cite Faidon Magkos, On adaptive thermogenesis: just another weight-loss tale?
Select Format Select format. Permissions Icon Permissions. Open in new tab Download slide. Google Scholar Crossref. Search ADS. Google Scholar PubMed. Ravussin et al. More relevant to this review, is the relationship between low rates of energy expenditure and the maintenance of a reduced body weight. Along these lines, it has been shown that individuals who regain the most weight over a month follow-up are also those in whom the greatest depression in h energy expenditure is witnessed during the weight-loss intervention.
In fact, greater reductions in energy expenditure may increase the degree of difficulty to bridge the gap with a manageable EI, as weight loss also increases appetite, 4 food reward and palatability of foods 68 as mentioned previously. Then, addressing whether or not the greater-than-predicted changes in energy expenditure persist in the weight-reduced state, if somehow individuals manage to maintain weight stability after weight loss, becomes interesting and important.
The re-analysis of the semi-starvation data from the classic experiment of Keys et al. Although these data support the existence of a depression in energy expenditure that persists beyond the energy restriction, under conditions where individuals are consuming food ad libitum after weight loss, it may be argued that this effect may be a carry-over from subjects having been recently semi-starved.
Through the meta-analysis approach, Astrup et al. They compiled results from formerly obese women who were compared with women who had never been obese. Results from the analyses showed that resting energy expenditure was 5. Unfortunately, little information was provided as to the time at which the post weight-loss assessment of energy expenditure was performed in the formerly obese subjects.
Collectively, these results underline the possibility that the metabolic adaptations that occur in response to prolonged energy deficit persist in time and that constant efforts may need to be deployed in the form of increased energy expenditure from exercise or strict adherence to lowered EI, similar to the characteristics of successful long-term weight-loss maintainers. As presented and discussed in this review, the increase in the drive to eat and the seemingly persistent depression of different components of energy expenditure after weight loss, may well complicate the maintenance of energy balance at that point, which is supported by the overwhelming level of weight relapse.
These observations provide an interesting platform for investigating approaches that may normalize weight-loss-induced effects on energy balance. Some studies have investigated the potential of exogenous leptin administration to attenuate the effects of weight loss on appetite and changes in energy expenditure. In the first of these two studies, it was reported that administrating recombinant leptin to human subjects after weight loss partly corrected some of the weight-loss-induced defects in energy expenditure.
Whether or not this approach would lead to improved long-term weight stability after weight loss remains to be determined. In conclusion, the observations presented and discussed in this paper indicate that a decrease in thermogenesis may occur in obese individuals maintaining a supervised diet—exercise program promoting weight loss.
This adaptation explains a substantial decrease in daily energy needs and is related to changes in appetite sensations promoting compensation possibly through increased EI.
As these thermogenic changes would seem to persist over time, they likely contribute to body weight regain following body weight loss. It thus seems important to further investigate adaptive thermogenesis in humans, be it for the development of relevant biomarkers or to improve diagnosis about individual determinants of the predisposition to obesity.
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Toxicol Sci ; 67 : 46— Thermogenesis and weight loss in obese individuals: a primary association with organochlorine pollution. The response to long-term overfeeding in identical twins. In humans, diet-induced thermogenesis is related to postprandial substrate metabolism of FFM with a questionable role of BAT. Thus, AT cannot be considered as unique. Conclusions: AT should be characterized based on individual components of daily energy expenditure, detailed body composition analyses, and mathematical modeling.
The biological basis of AT as well as the influences of age, sex, obesity, stress, and inflammation remain to be established in humans.
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