PHB-09498; No of Pages 6

Physiology & Behavior xxx (2011) xxx–xxx

Contents lists available at ScienceDirect

Physiology & Behavior

j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / p h b

Obesity: The allostatic load of weight loss dieting

Angelo Tremblay a,⁎, Jean-Philippe Chaput b
a
Division of Kinesiology, Faculty of Medicine, Laval University, Quebec City, QC, Canada, G1V 0A6
b
Healthy Active Living and Obesity Research Group, Children's Hospital of Eastern Ontario Research Institute, Ottawa, ON, Canada, K1H 8L1

a r t i c l e i n f o a b s t r a c t

Article history: The obesity epidemic that is prevailing in most countries of the world is generally attributed to the increased
Received 30 March 2011 amount of opportunities to be in positive energy balance in a context of modernity. This obviously refers not
Received in revised form 11 May 2011 only to sedentariness and unhealthy eating that may dominate life habits of many individuals but also to
Accepted 16 May 2011
unsuspected non-caloric factors which produce discrete allostatic changes in the body. In this paper, the focus
Available online xxxx
is put on the impact of some of these factors with the preoccupation to document the allostatic burden of
Keywords:
weight loss. Thus, beyond the fact that modernity favors opportunities to eat much and not to be active, the
Energy balance proposed conceptual integration leads to the conclusion that a modern lifestyle makes weight loss more
Homeostasis difficult for obese individuals. In addition to the natural effects of weight loss favoring resistance to lose fat, a
Pollutant lifestyle promoting shorter sleep duration and more cognitive demand produces allostatic changes that may
Sleep duration interfere with weight loss. The case of persistent organic pollutants (POPs) is also discussed as an example of
Mental work the potential detrimental effects of a contaminated environment on metabolic processes involved in the
control of energy expenditure. Taken together, these observations suggest that weight loss is more than ever a
search for compromise between its metabolic benefits and its allostatic effects promoting body weight regain.
© 2011 Elsevier Inc. All rights reserved.

The epidemic of obesity that has been described by the World
Health Organization more than a decade ago has over-emphasized the
use of weight loss dieting that has traditionally been prescribed
as the first modality to treat obesity. According to the first law of
thermodynamics, food restriction spontaneously creates a negative
energy balance that is associated with an improvement of the meta-
bolic profile of obese individuals. Indeed, there is a consensus in the
scientific literature regarding the beneficial effects of weight loss on
energy metabolism, particularly the variables which are biomarkers of
the metabolic syndrome. Our research and clinical experience reveal
that weight loss of several kilos is sufficient to decrease plasma levels
of glucose, insulin, and lipid-lipoproteins as well as systolic and
diastolic blood pressure [1]. Our experience also indicates that these
benefits are not proportional to weight loss. Beyond a threshold of 5 to
10 kg weight loss, the metabolic benefits may become non signifi-
cant [2,3]. On the other hand, this threshold might also represent the
limit beyond which some less desirable physiological adaptations are
observed. As discussed in this paper, the allostatic load of a large
weight loss can be important and may promote a physiological
disturbance favoring weight regain. In addition, evidence is presented
about the possibility that such a disturbance may be exacerbated in
the daily activity context of modernization and globalization.
⁎ Corresponding author at: Division of Kinesiology, PEPS, room 0234, Laval
University, Quebec City (Quebec), Canada, G1V 0A6. Tel.: +1 418 656 7294; fax: + 1
418 656 3044.
E-mail address: angelo.tremblay@kin.msp.ulaval.ca (A. Tremblay).
1. The RQ–FQ balance
Variations in fat mass have been shown to influence fat mo-
bilization and oxidation. Many years ago, Bjorntorp et al. [4] doc-
umented the existence of a relationship between the expansion of fat
mass and free-fatty acid levels and turnover. In a subsequent study by
Schutz et al. [5], it was shown that a significant relationship exists
between variations in fat mass and those in resting lipid oxidation.
Specifically, these authors deduced from their cross-sectional obser-
vations that a change of 10 kg in fat mass was positively related to a
change of 20 g per day in resting lipid oxidation. These findings thus
imply that fluctuations in body fat are associated with changes in
fat oxidation that should normally result in a new fat balance, i.e. a
threshold of equilibrium between fat intake and oxidation at a
reduced level, following a weight loss program.
The demonstration by Flatt et al. [6] that fat oxidation is not
responsive to an acute increase in fat intake represented the corner
stone of the justification integrating the above referenced observa-
tions into an allostatic mechanism that was called the RQ–FQ balance
[7]. In brief, this notion stipulates that energy balance occurs in both
animals and humans when macronutrient balance is achieved. This
balance represents the equilibrium between respiratory quotient
(RQ), a marker of the composition of the fuel mix oxidized, and food
quotient (FQ) which is an indicator of the macronutrient composition
of the diet. This concept also considers each macronutrient compo-
nent of the substrate balance, i.e. protein, carbohydrate and fat
balances. As described by Flatt [8], amino acid and glucose oxidation

0031-9384/$ – see front matter © 2011 Elsevier Inc. All rights reserved.
doi:10.1016/j.physbeh.2011.05.020

Please cite this article as: Tremblay A, Chaput J-P, Obesity: The allostatic load of weight loss dieting, Physiol Behav (2011), doi:10.1016/
j.physbeh.2011.05.020
2 A. Tremblay, J.-P. Chaput / Physiology & Behavior xxx (2011) xxx–xxx
rates are acutely adjusted to the amounts of protein and carbohydrate
consumed. Since this mechanism does not seem to exist for fat
metabolism [6], fat oxidation is primarily determined by the gap
between daily energy expenditure and the amount of energy ingested
as carbohydrates and proteins [8]. Taken together, these observations
emphasize the relative vulnerability of fat balance to substantial
fluctuations in energy/fat intake due to its inaccurate regulation. In
fact, as indicated above, this regulation is performed on a more long
term basis compared to proteins and carbohydrates and it seems to
partly operate in proportion to changes in body fat mass.
The RQ–FQ concept is important for health professionals relying on
weight loss dieting to modify body composition in obese individuals.
Indeed, this concept implies that fat oxidation decreases over time
proportionally with fat loss and that a threshold will occur beyond
which it will not be possible to maintain fat balance even if the patient
strictly adheres to a fat-reduced diet. In other words, “fat burning” in
the weight-reduced obese individuals might become sufficiently low
not to permit an equilibrium between fat intake and fat oxidation. In
such a context, the spontaneous question to be addressed pertains to
the possibility to compensate for the decreased ability of a reduced fat
mass to support lipid oxidation. As described by Flatt [7], exercise then
becomes the primary lifestyle modality to stimulate lipid metabolism.
Indeed, physical activity can acutely increase fat oxidation [9] and
can contribute to maintain a reduced body weight up to certain limits
which are fixed by the balance between the enhancing effect of
exercise and the reducing effect of fat loss on lipid mobilization/ox-
idation. For instance, ex-obese long distance runners were able to
maintain a mean weight loss of 39 kg by mostly relying on an exercise
program including 90 km of running per week [10]. At that time, their
demanding training program was at best allowing the maintenance of
their fat cell lipolysis at the level of their lean sedentary controls. This
is concordant with the observation made in elite female swimmers
who gained 4 kg of body fat (equivalent to about 600 kcal per day)
within 2 months following an intensive training program aimed at a
participation in Olympic Games [11]. These results obtained in
athletes are also relevant for the treatment of obese individuals. In
the first clinical study in which we have tried to apply the RQ–FQ
concept in the clinical management of obesity, obese women were
subjected to a low fat diet and an aerobic training program up to the
occurrence of resistance to lose fat. In the most successful participants,
resistance to further lose fat occurred after a 15 kg weight loss [12].
Interestingly, when resistance to fat loss was observed, subjects were
less able to maintain their full adherence to the prescribed dietary
regimen and this did not appear to be due to their lack of discipline
and commitment. Indeed, the examination of their reported energy
intake data revealed that at resistance to lose fat, they were main-
taining their low energy intake. However, our estimates of daily
energy needs were then imposing a further decrease in prescribed
energy/lipid intake that subjects were not able to follow.
The RQ–FQ concept also imposes to take into account the ability of
obesity-prone individuals to use body fat as an energy substrate. In
general, obese individuals displaying a stable body weight oxidize
more fat when expressed in absolute terms. As indicated above, this is
at least partly explained by the enhancing effect of fat gain on lipid
oxidation [5]. However, when these individuals are tested following a
substantial weight loss, their metabolic capacity regarding fat uti-
lization seems to be lower than their controls paired for body weight.
Specifically, a lower fat oxidation level was observed in reduced obese
persons [13]. Moreover, formerly obese [14] and obese [15] subjects
were found to be less responsive to lipid oxidation when exposed to
increased fat intake. Specifically, this means that obesity prone
individuals may need in the long run a more pronounced fat gain
before reaching a new fat balance under high fat diet conditions. Along
these lines, it is also noteworthy to emphasize that a high 24-h RQ,
reflecting a reduced relative fat oxidation, was shown to be predictive
of a higher risk to gain body weight during subsequent years [16,17].
Please cite this article as: Tremblay A, Chaput J-P, Obesity: The allostatic load of weight loss dieting, Physiol Behav (2011), doi:10.1016/
j.physbeh.2011.05.020
In summary, the RQ–FQ balance concept and the emphasis that it
gives to the regulation of fat balance are worth of consideration in any
discussion of the allostatic load of weight loss dieting. Indeed, the
adjustment in fat oxidation that occurs with weight loss should be
viewed as a solution of re-equilibration in order to preserve body
energy as fat. Specifically, this implies that this decrease in fat oxi-
dation can become a determinant of the inability to subsequently lose
body weight. As further discussed, the effects of weight loss on fat
metabolism might also underlie some allostatic perturbations in
carbohydrate metabolism.
2. Body weight loss and mild hypoglycemia
The regulation of glycemia is an issue that health professionals
generally consider as being related to the risk of hyperglycemia and
ultimately diabetes. Accordingly, weight loss dieting is almost system-
atically justified by the need to improve the metabolic profile of the
obese, including the decrease of hyperglycemia towards a normal
glycemic state. However, precise regulation of plasma glucose levels also
imposes the prevention of hypoglycemia. In this regard, Mayer [18]
proposed a glucostatic theory of food intake control that is based on the
idea that reduced glucose utilization in the brain represents a stimulus
that is detected by glucosensitive brain sites and that can influence
appetite sensations. In addition, Mayer [19] argued that this theory
could account for short term variations in hunger and food intake
whereas he proposed that a lipostatic mechanism, such as that
described above, could explain long term variations in energy balance.
In a recent paper [20], we have reviewed evidence pertaining to the
clinical implications of this theory, with a particular focus on body
weight variations. Although Mayer's hypothesis has some limitations, it
at least provided us a conceptual basis for further investigations by our
research group.
The follow-up of subjects tested in phases 2 and 3 of the Quebec
Family Study allowed a prospective analysis of the relationship between
glucose concentrations at the end of an oral glucose tolerance test
(OGTT) and changes in body weight over a 6-year follow-up period [21].
In this study, we observed that glucose concentrations at 120 min of the
OGTT were negatively correlated with weight gain over time, indicating
that the proneness to reactive hypoglycemia was predictive of a
more pronounced weight gain in the long run. We also tested obese
individuals subjected to a 15-week weight-reducing program. Again,
the focus of this study was the association between glycemic stability
and weight gain which was recorded over a mean follow-up of 81 weeks
after the weight loss dieting treatment. The results showed that the
glucose area below fasting values (a standardized index of reactive
hypoglycemia during an OGTT) increased significantly after weight loss
and was significantly correlated with weight regain [21]. To summarize,
our clinical experience revealed that reduced glucose concentrations at
the end of an OGTT were correlated with weight gain over time and with
the amount of weight regained after weight loss. Although these results
tend to support Mayer's hypothesis, it might also be attributed to
endocrine changes in response to food/glucose intake that induced mild
hypoglycemia and promoted weight gain. Because insulin generally
promotes fat storage, postprandial hyperinsulinemia might also explain
weight gain in individuals experiencing mild hypoglycemia.
We have also performed several studies to evaluate the impact of
weight loss up to a resistance threshold to fat loss on glucose ho-
meostasis. In the first study of this series, obese women were sub-
jected to an intervention based on the RQ–FQ concept, i.e. a low fat
diet and an exercise program, up to the occurrence of fat loss plateau
[12]. At that time, their health-related metabolic profile was
normalized even if they still displayed a BMI typical of an obese
state. Furthermore, the examination of their glucose curve during the
OGTT revealed a proneness to mild hypoglycemia at the end of the
intervention. The repetition of this treatment approach in both obese
men and women who were also tested up to resistance to lose fat
 A. Tremblay, J.-P. Chaput / Physiology & Behavior xxx (2011) xxx–xxx
confirmed the manifestation of reactive hypoglycemia following a
substantial fat loss [22].
To further validate the hypothesis of an increased risk of reactive
hypoglycemia promoted by weight loss dieting, we designed a se-
quential therapeutic approach requiring the testing of male obese
subjects at every 5 kg of weight loss and at resistance to fat loss.
According to our previous experience, the treatment was based on
low fat diet and exercise. This protocol induced weight loss in the
participants who became resistant to lose fat after an 11 kg weight
loss [23]. As expected, reactive hypoglycemia at the end of the OGTT
was accentuated following the program. In addition, we used this
protocol to evaluate some clinical implications of the allostatic
changes found in this study. As illustrated in Fig. 1, changes in the
area of plasma glucose below basal levels were related to those of the
Beck Depression Inventory score. Apart from an increase in depression
symptoms as a result of weight loss dieting [23], recent results have
shown that dieting increases psychological stress and cortisol pro-
duction in women [24], suggesting that we may have to rethink
recommending dieting as a means of improving health.
These observations demonstrate that weight loss up to the point of
apparent resistance to further lose fat disrupts glucose homeostasis in
a way that promotes weight regain in previously obese individuals.
This increased predisposition to hypoglycemia might explain the state
of hyperglucagonemia that was found to persist in weight-reduced
obese individuals [25]. Moreover, recent data of the Quebec Family
Study showed that an increase in the area of plasma glucose below
basal levels is an independent predictor of the risk to develop glucose
intolerance/diabetes over a 6-year follow-up period [26].
In summary, it seems that weight loss dieting should be perceived
as a matter of compromise between the benefits of a small to mod-
erate weight loss and the physiological vulnerability that is conferred
by a moderate to large weight loss. As discussed in the next section,
this perception is maybe even more relevant in a context of modernity
where the lifestyle clearly promotes undesirable effects on the
regulation of energy metabolism.
3. Metabolic allostasis and body weight stability in a
modern environment
The modern way of living appears to impose a tremendous
challenge to anybody who wants to remain lean — it encourages the
consumption of energy and discourages the expenditure of energy.
The high prevalence of obesity appears fundamentally linked to our
so-called “obesogenic environment” — high stress levels, lack of sleep,
abundant supplies of cheap, highly palatable, energy-dense foods,
automation and elimination of physical activity from our homes and
workplaces, dependence on powered transportation instead of our
12
r = –0.77
Δ BDI (arbitrary units)
9 neuroglycopenia and impaired mood, which was corrected by the
P < 0.01
6 pothesis that “comfort food” reduces the activity of the stress system
3 sympatho-adrenal responses, which were not affected by exogenous
0 stress-induced mood changes were resolved by food ingestion cannot
-3 -2.5 -2 -1.5 -1
-3
Δ Glucose (mmol/L)
Fig. 1. Association between change in glucose concentrations at 180 min of the oral
glucose challenge and change in Beck Depression Inventory scores. The change is the
difference between plateau and baseline values. Figure reproduced with permission
from Chaput et al. [23].
Please cite this article as: Tremblay A, Chaput J-P, Obesity: The allostatic load of weight loss dieting, Physiol Behav (2011), doi:10.1016/
j.physbeh.2011.05.020
3
feet, etc. Unfortunately, these conditions are unlikely to be reversed in
the short term. It is important to realize that the excess weight
gain observed in prone individuals should be perceived as a normal
physiological adaptation to a changed environment, rather than a
malfunction of the regulatory system [27,28]. Accordingly, prevention
and treatment strategies for obesity should ideally focus on modifying
the root causes of weight gain. Furthermore, it is important to better
understand the implications of this new reality of living on metabolic
allostasis, appetite control and ultimately body weight. This better
understanding is crucial if we want to increase our chances of success
in any dietary intervention aimed at losing weight.
Technological advances that occurred over the past 30 years, par-
ticularly with respect to electronic engineering and computer
sciences, have increased the demand for mental activities (as opposed
to physical activities). As recently reported [29], we are only starting
to document the implications of mental work on energy metabolism
and it seems that these implications far exceed those associated with a
lack of physical activity. Indeed, a careful examination of computer-
related activities reveals that they represent a particular type of
sedentary activities — they are stressful and biologically demanding
for the body [30]. Recent experimental studies have shown that
computer-based activities increase ad libitum food intake without
increased sensations of hunger [31,32]. These results agree with a
study involving scientists from the University of Washington who
increased their energy and fat intake at the time of the preparation of
NIH grant applications [33]. These results are also concordant with
recent studies showing that television viewing and video game
playing stimulate food intake despite their low “calorie-burning”
nature [34]. Moreover, cognitive work acutely induced increased
fluctuations in plasma glucose and insulin levels compared with a
control, resting condition [32]. In accordance with the glucostatic
theory of appetite control, the increased variability of glycemia was
related to a compensatory increase in energy intake [20]. Interest-
ingly, we also observed that mental work produced an increase in
cortisol levels which was related to a compensatory increase in food
intake [35]. Future studies will be necessary to better clarify the
underlying mechanisms and to determine the relative contribution of
homeostatic (hormonal signals that trigger food intake) vs. non-
homeostatic (eating in the absence of hunger) feeding behaviors.
The “selfish brain” theory [36] is another interesting concept that has
recently received attention in providing a more complete understanding
of the brain's priority in energy metabolism. During acute mild mental
stress, the energy supply of the human brain increases by 12% [37]. In an
attempt to better understand this phenomenon, Hitze and colleagues
[38] recently reported that the brain under mental stress demands for
energy from the body by making use of cerebral insulin suppression.
Additionally, cognitive demand did also increase the brain's energy
need. After psychological stress, energy intake was found markedly
increased to supply the brain and the body with energy for re-
plenishment [38]. Interestingly, changes in cerebral energy state were
parallel to the changes in mood. Mental stress induced a state of both
supplementation of exogenous energy. However, contrary to the hy-
and thereby relieves bad mood [39], the subjects displayed robust
energy (either orally or intravenously). Thus, the fact that mental-
be attributed to changes in the stress system but it rather indicates that
mood was restored by restoring cerebral energy homeostasis [38].
Lack of sleep is another feature of our modern lifestyle that has
been shown to be a metabolic stressor. Indeed, sleep curtailment has
become an endemic condition of modern societies, with population
statistics revealing that sleep duration has decreased by more than 1 h
over the last few decades [40]. The proof-of-concept for short sleep
duration as a possible cause of obesity is growing. Prospective cohort
4 A. Tremblay, J.-P. Chaput / Physiology & Behavior xxx (2011) xxx–xxx
studies have shown that short sleep duration is associated with
weight gain and an increased incidence of obesity in children and
adults [41,42]. Intervention studies have provided a mechanistic
explanation for the short sleep-obesity connection (i.e. that sleep
restriction impacts hormonal control of appetite). Indeed, lack of sleep
has been reported to decrease plasma leptin levels, increase plasma
ghrelin and cortisol levels, alter glucose homeostasis, and activate the
orexin system, all of which impact the control of appetite [43–45].
Interestingly, we have recently shown that short sleepers present
lower glucose concentrations at the end of an OGTT [46], thereby
providing another potential explanation on the basis of the glucostatic
theory of appetite control (Fig. 2). Besides, the increased time and
opportunities for eating as well as the increased fatigue associated
with lack of sleep are other explanations that have been proposed
[47]. Hence, a good night's sleep is expected to favor a good coupling
between energy input and output and should be encouraged in the
prevention of weight gain. Future research is needed to determine
whether sleep extension in sleep-deprived obese individuals will
influence appetite control and/or reduce the amount of body fat. In
this regard, we recently observed that a change towards longer sleep
duration promoted the interruption of excess weight gain in short
sleepers [48]. We also have to keep in mind that lack of sleep can be a
symptom of chronic stress or typical depression. In this context,
chronic stress would lead to impaired sleep on the one hand, and the
adaptation to chronic stress would lead to weight gain on the other
hand.
In the context of weight loss, dietary restriction is widely used as a
means of inducing a caloric deficit. However, recent evidence suggests
that adequate sleep might be an important factor in successful weight
loss, and perhaps sleep should be included as part of the lifestyle
package that traditionally has focused on diet and exercise [49]. In this
crossover study, overweight adults were randomly assigned to sleep
either 5.5 h or 8.5 h each night for 14 days in conjunction with
moderate caloric restriction in a closed clinical research environment.
The authors found that the participants lost the same amount of
weight under both conditions; however, sleep restriction decreased
the proportion of weight lost of fat by 55% and increased the loss of
fat-free mass by 60%. Fat oxidation was lower in the sleep-deprived
state, and ghrelin and hunger levels were also found to be higher with
sleep deprivation. These findings are novel and suggest that getting
too little sleep might prevent dieters from losing as much body fat as
they otherwise would have.
Altogether, the modern way of living has many implications on
energy metabolism and we should pay particular attention to this new
reality. As discussed in this section, mental stress (either in the forms
of cognitive working, television viewing or video game playing) and
unrestorative sleep can partly explain the inter-individual variability
70
*
GABF (mmol/L x min)
60
50
40
30
20
10
0
Short sleepers Average sleepers
Fig. 2. Mean glucose area below fasting glucose levels for short (5–6 h) and average (7–8 h)
adult sleepers involved in the Quebec Family Study. Data are expressed as means± SEM.
GABF: glucose area below fasting glucose concentrations. *Significantly different from
average sleepers (P b 0.01).
Adapted from Chaput et al. [46].
Please cite this article as: Tremblay A, Chaput J-P, Obesity: The allostatic load of weight loss dieting, Physiol Behav (2011), doi:10.1016/
j.physbeh.2011.05.020
in response to diet-induced weight loss. Targeting the root causes of
weight gain will definitively improve our chances of success.
4. Weight loss and the allostatic burden of
environmental pollutants
The weight gain observed over recent years has been shown to
occur not only in humans but also in various animal species [50]. Since
the usually advocated “Big Two” factors [51] to explain obesity, i.e.
sedentariness and unhealthy macronutrient diet composition, cannot
explain weight gain in some animals, this has raised the hypothesis
that common unsuspected environmental factors may underly weight
gain in humans and animals [51]. Among these factors, lipid soluble
persistent organic pollutants (POPs) have frequently been pointed out
as potential determinant of allostatic changes promoting obesity.
POPs are endocrine-disrupting chemicals and include polychlorinated
biphenyls (PCBs) and organochlorine pesticides. Despite the ban on
their use in several countries including Canada and the United States,
their stability, resistance to degradation, and lipophilicity has led to
significant bioaccumulation in most compartments of the ecosystem
and human tissues [52]. This bioaccumulation leads to an ongoing
human exposure to POPs through several pathways (food intake
being the main one), so the present concentration of POPs in serum
reflects both a release from fat storage compartments as well as an
uptake from present exposure. It has recently been shown that low
levels of polychlorinated biphenyl-77 increase adipocyte differentia-
tion, promote the expression of proinflammatory adipokines, and
augment the expression of the peroxisome proliferator-activated re-
ceptor γ, a key promoter in regulating cell energy homeostasis
[53,54]. Thus, these data suggest that even low-level exposure to POPs,
as observed today in the human population, might have obesogenic
effects.
Lim et al. [55] have recently reexamined this issue in a large
population study by analyzing the relationship between serum con-
centrations of POPs and weight gain over 1 and 10 years. The results
showed that POPs concentrations were higher in individuals with long
term weight loss (due to a hyperconcentration of POPs in serum as a
result of fat loss) whereas they were lower in those with a history of
long term weight gain. Although both beneficial health effects after
weight loss and harmful health effects after weight gain are generally
expected, changes in serum concentrations of POPs in relation to
weight change may act on health in directions opposite to what we
expect with weight change. This then highlights another contribution
of adipose tissue to body homeostasis due to its ability to store and
then dilute POPs with the beneficial consequence to reduce their
exposure to other tissues. In fact, as further explained in this section,
this effect becomes more apparent during weight loss which can then
be described as a decrease in the storage space of POPs.
To our knowledge, Backman and Kolmodin-Hedman [56] were the
first investigators to demonstrate the enhancing effect of a sub-
stantial fat loss on circulating concentrations of POPs. Over the last
decade, we have pursued the study of this issue with the preoccu-
pation to identify some allostatic consequences of the weight loss-
induced changes in plasma POPs concentrations. As expected, we
observed a significant increase in POPs concentrations after a weight
loss of about 10 kg in obese individuals [57]. This increase was highly
correlated with that of POPs concentrations [58] in adipose tissue and
was also associated with a greater than predicted decrease in skeletal
muscle oxidative enzymes [59], plasma triiodothyronine and resting
metabolic rate (RMR) [60], and sleeping metabolic rate (SMR) [61].
The use of an ANOVA in this context also showed that changes in
plasma concentrations of POPs were the best predictor of changes in
RMR [60] and SMR [61] in response to the weight-reducing program.
Taken together, these observations provide an indication of the
vulnerability of the control of energy expenditure that is promoted by
body weight loss. This is concordant with the arguments of Lim et al.
 A. Tremblay, J.-P. Chaput / Physiology & Behavior xxx (2011) xxx–xxx
[55] who emphasized that many observational studies have reported
that weight loss was associated with increased risk of some diseases
and total mortality. It thus seems that environmental pollution creates
a paradox by which fat gain becomes protective against the body
burden imposed by a contaminated environment.
5. Conclusions
This paper presents some observations pertaining to the allostatic
burden of body weight loss that help in understanding the difficulties
experienced by obese persons in their attempt to normalize their
body weight. On one hand, it seems that weight loss naturally favors
metabolic changes that ultimately lead to resistance to further lose fat
and maybe weight regain. Second, evidence supports the idea that our
modern way of living characterized by reduced sleep duration and
more demanding cognitive effort can interfere with the outcome of a
weight loss attempt. Finally, from an ecological standpoint, fat loss
involves a reduction of the anti-toxins protective role of adipose tissue
that is related to its capacity to dilute POPs. Thus, in response to
weight loss dieting, the resulting allostatic changes globally favor a
decreased potential of the body's metabolic “furnace” and of the
ability to spontaneously match energy intake and expenditure.
Acknowledgments
The research reported in this paper was partly funded by the
Canada Research Chair in Environment and Energy Balance.
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Please cite this article as: Tremblay A, Chaput J-P, Obesity: The allostatic load of weight loss dieting, Physiol Behav (2011), doi:10.1016/
j.physbeh.2011.05.020