Metabolic Adaptations To Weight Loss A Brief.39

Brief Review
Metabolic Adaptations to Weight Loss: A Brief

Review
Mario G. Martı́nez-Gómez,1 and Brandon M. Roberts2
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1
CarloSportNutrition, Spain; and 2University of Alabama at Birmingham, Birmingham, Alabama
CX1AWnYQp/IlQrHD3i3D0OdRyi7TvSFl4Cf3VC4/OAVpDDa8KKGKV0Ymy+78= on 04/15/2024
Abstract
Martı́nez-Gómez, MG and Roberts, BM. Metabolic adaptations to weight loss: A brief review. J Strength Cond Res 36(10):
2970–2981, 2022—As the scientific literature has continuously shown, body mass loss attempts do not always follow a linear
fashion nor always go as expected even when the intervention is calculated with precise tools. One of the main reasons why this
tends to happen relies on our body’s biological drive to regain the body mass we lose to survive. This phenomenon has been
referred to as “metabolic adaptation” many times in the literature and plays a very relevant role in the management of obesity and
human weight loss. This review will provide insights into some of the theoretical models for the etiology of metabolic adaptation as
well as a quick look into the physiological and endocrine mechanisms that underlie it. Nutritional strategies and dietetic tools are
thus necessary to confront these so-called adaptations to body mass loss. Among some of these strategies, we can highlight
increasing protein needs, opting for high-fiber foods or programming-controlled diet refeeds, and diet breaks over a large body
mass loss phase. Outside the nutritional aspects, it might be wise to increase the physical activity and thus the energy flux of an
individual when possible to maintain diet-induced body mass loss in the long term. This review will examine these protocols and their
viability in the context of adherence and sustainability for the individual toward successful body mass loss.
Key Words: body mass loss, caloric restriction, adaptative thermogenesis, appetite control, energy intake, metabolic rate, diet
refeeds, diet breaks
Introduction magnitude of the energy deficit, where higher deficits will promote
larger homeostatic responses; or previous body composition, where
Energy balance could be described as the resultant difference from the
lower body fat levels before the intervention will result in more drastic
number of calories consumed by an individual through food intake
metabolic adaptations (159,194). It also remains unclearly answered
and the energy expended to maintain his metabolic and physiological
whether certain nutritional interventions can reduce the severity of the
functions and support physical activity and exercise demands (76). If
adaptations to body mass loss because the available evidence is re-
we conceive the human body as a bioenergetic system, this concept
duced, restricted to specific populations (overweight individuals) and
would align with the first law of thermodynamics, which postures
many studies are performed in mice (71,74). Inferring practical ap-
that the total energy of a system is constant, where energy can be
plications from these data may be of relevance for both researchers
transformed from one form to another but cannot be created nor
and practitioners to achieve successful body mass loss in populations
destroyed. Thus, modifications over the course of time in energy
who might struggle at manipulating body mass for various reasons
balance would be the prime determinant of body mass variation in
(obese individuals, athletes, etc).
humans (77). Alongside this concept, successful body mass loss in an
It is thus important to understand (a) the dynamic nature of
individual can be achieved by creating what is known as a caloric
energy balance, (b) how these series of “metabolic adaptations”
deficit or energy deficit, which, broadly speaking, consists of
can affect body mass loss and body mass regain over time, and (c)
expending more calories or energy than those ingested through food
what are the possible nutritional solutions proposed to mitigate
either by increasing physical activity or decreasing one’s caloric intake
these phenomena. These will be the main aims of this review.
(181). Despite the promotion of different types of diets for body mass
loss (68,135), the weekly application of the aforementioned principle
(energy deficit) is common among all of them and remains the prime Evolutionary Origins and Models to
determinant factor for body mass reduction (188). Nonetheless, this Metabolic Adaptation
process is not expected to occur linearly (66,96) because it is well
documented that macronutrient distribution can affect the magnitude The question still arises as to why our species have been endowed with
of losses in the short term (100) and that a series of homeostatic and these modifications to our physiology during periods of energy re-
metabolic adaptations, such as adaptive thermogenesis (AT) (172), striction. Although the answer is still inconclusive and mostly de-
changes in mitochondrial efficiency (14), or alterations in the levels of pendent on multiple factors, some hypotheses related to our
circulating hormones occur during periods of energy restriction (147). evolutionary past have been postulated. The “Thrifty gene hypothe-
The severity of these changes will depend on the duration of the sis” states that several thousand years back, environmental pressures
dieting period, where longer durations will increase adaptations; the and natural selection would favor those who were able to survive long
periods of famine when food was scarce, and thus are the ones who
Address correspondence to Brandon M. Roberts, Brob21@uab.edu. prevailed and conform our genetic heritage, a heritage that when
Journal of Strength and Conditioning Research 36(10)/2970–2981 thrown in our modern “obesogenic environment” lead us to chronic
ª 2021 National Strength and Conditioning Association disease (155). In simple words, “Our ancient savior has become our
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Metabolic Adaptation to Body Mass Loss (2022) 36:10 | www.nsca.com
modern issue.” Although this theory is an oversimplification that cases, with an average contribution of 70% to TDEE (127). This
takes a determinist standpoint and only provides a causal genetic value will depend on many variables such as sex, height, age, physical
factor for the development of obesity in our era, it can be used as a activity, and other factors (2,46,91). It is mostly static through an
conceptual framework to understand why metabolic adaptation oc- individual’s lifetime, with losses or gains in metabolically active tissue
curs and where it could have come from. Another hypothesis that such as lean body mass (LBM) contributing to a small effect (141)
aligns with this last one to explain the issue at hand is the existence of along with variations in REE (118,151). Other factors, such as re-
a “hypothalamic feeding center,” more commonly referred as “adi- sistance exercise, can minimally increase REE (131). For research
postat,” an axis between all of our organs and our central nervous purposes, it should be minded that after approximately 2 days of
system that would tightly control food intake in the long term fasting, transient increases in this component (5–10%) can be ob-
(40,180). This system would receive afferent signals ranging from served because of an increase in the gluconeogenesis rate (185).
hormones (leptin, ghrelin, insulin, etc) to the gut or adipose tissue that The second component is non-REE that is further divided into
would help to establish a “set-point” of energy reserves primarily in other 3 contributors: exercise activity thermogenesis (EAT), non-
the form of adipose tissue and hepatic and muscular glycogen storage EAT (NEAT), and the thermic effect of food (TEF).
thresholds (105,110). This hypothesis has been generally accepted by Thermic effect of food refers to the energy expended during the
the scientific community as a theoretical model to understand the self- digestion of food, and its contribution to TDEE is estimated to be
regulation of food intake but presents several limitations to explain around 10%. However, it should be noted that different macro-
certain diseases, such as obesity (30). The focus of the theoretical nutrients as well as other variables (size of meals, processing of
models for food intake regulation, however, has not only been placed foods, and duration) contribute separately to this effect, where
on adipose tissue; Millward proposed the existence of a “protein- bigger meals and higher carbohydrate and protein contents can
stat” that would suggest food intake to be regulated through the have a larger impact on TEF (25). This factor might be of con-
needs for maintenance of lean mass (145). According to Millward, the sideration when accounting for the TDEE of specific populations,
impetus for lean tissue growth and the need for muscle tissue repletion for instance, high-protein diets for some athletes (156). However,
after malnourishment conditions become key variables in de- some metabolic chamber studies in overweight subjects show that
termining appetite and meal size. Although, the evidence for this even high-protein feedings may not pose a significant difference in
hypothesis is largely based on mechanistic data, later studies have TDEE (17), contrary to what could be expected. A commonly
established a strong relationship between fat-free mass (FFM) losses held myth regarding TEF is that a higher frequency of meals will
and compensatory responses to body mass loss. Regarding AT, Keys result in increased thermogenesis, but research does not support
et al. were the first ones to define this event (146). Adaptive ther- this claim (114), and in fact, some may suggest the opposite (167).
mogenesis is explained as a spontaneous decrease in energy expen- Exercise activity thermogenesis would refer to the energy
diture (EE) during body mass loss, potentially coming from expended during daily, programmed exercise sessions. This value
reductions in the metabolic rate of some relevant organs (heart, kid- accounts for little for TDEE (5–10%) and remains unchanged for
neys, brain, or liver) and tissues contained within the FFM (141). In the most part unless exercise is ceased or the body mass of an
another important study on this topic (150), it was reported the individual is reduced significantly (54), thus needing less energy to
magnitude of the adaptation to be around 70–100 kcal·d21. Al- support the locomotion required to perform.
though clinically significant, we must take these data with caution Non-EAT is defined as the energy required to support nonexercise-
because FFM is widely varied in respect to its composition (193), and related tasks, such as walking and other leisure time activities
adjusting for variables such as the water content of different organs (38,124). This component has gathered a lot of attention in recent
and tissues might affect the previous calculation. Several methodo- years due to its large and variable contribution to TDEE. Non-EAT
logical limitations arise when accounting for the evaluation of AT has also been shown to downregulate during periods of energy re-
(20). Interindividual variability was also observed in the Minnesota striction (126) and even maintain that state afterward, potentially
experiment (150), where higher baseline EE was associated with contributing to body mass regain (202). However, a recent review on
higher AT, supporting the notion that the magnitude of body mass the topic (184), aimed to examine the response of NEAT to diet
loss can be proportional to AT. Nonetheless, the EE component interventions to promote body mass loss, concluding, despite having
(which will be further explained in better detail) where this reduced relevant limitations and a high risk of bias, did not support a signifi-
EE might come from remains unclear because AT might be explained cant reduction in these components. All TDEE contributors are sub-
from decreases in the nonresting energy compartment of EE (non- jected to some degree of both interindividual and within-individual
voluntary reductions in EE through decreases in physical activity), as variability (53), where the largest variations in TDEE are dictated by
other models have proposed (173). Considering this, whether AT is changes in NEAT. If we were to take NEAT into perspective with the
relevant itself or even actually measurable as part of the metabolic other components, it could represent 15% of TDEE in sedentary
adaptation to body mass loss remains disputed (56). In fact, recent subjects and up to 50% in more active individuals (124,125). Figure 1
studies by Martins et al. (139,140) support the idea that AT is only visually summarizes the different components of EE.
appreciable when subjects are in energy restriction conditions and
that its magnitude is not sufficient to explain body mass relapse in the
long term.
Physiological Responses to Body Mass Loss and
Endocrine Modulation of Food Intake
The energy balance equation remains undisputed for explaining
Components of Energy Expenditure
changes in an individual’s body mass. However, a series of physio-
A sustained energy deficit over time will lead to body mass loss, thus it logical and endocrine alterations occur in response to an energy
is important to describe the total daily EE (TDEE) of an individual deficit that can drive the behavioral response of an individual re-
(132). We can describe at least 2 major components that determine an garding appetite, satiety, and food intake, potentially closing the gap
individual’s TDEE. The first one, resting EE (REE), refers to the basal between the prescribed energy deficit and the actual caloric intake.
metabolic rate and will be the largest constituent of TDEE in most Some of the extreme attempts to reduce body mass can be observed in
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Metabolic Adaptation to Body Mass Loss (2022) 36:10
Figure 1. Components of TDEE and their reported coefficients of variation. Note how
daily exercise activity thermogenesis (EAT) is a far-less relevant contributor to TDEE
than nonprogrammed activity (NEAT), despite the common belief. Thermic effect of
food reports a high variability because it might be dependent on the properties of food
ingested. Adapted from various sources (53,132,194). TDEE 5 total daily energy
expenditure; REE 5 resting energy expenditure; TEF 5 thermic effect of food.
sports where body mass or esthetic appearance is relevant for per- reported that those who lost .5% of body mass experienced signifi-
formance outcomes (combat sports, gymnastics, and bodybuilding). cant reductions in T3 as well as in the T3: T4 ratio. Thyroid hormone
A series of observational and case-report data show many endocrine has also been shown to stimulate brown adipose tissue (19), which can
and hormonal alterations in athletes who undergo these practices make small contributions to EE (29) and is likely less present in obese
(99,157,174). These endocrine profile changes are generally rele- individuals (206).
gated to increases in orexigenic signals and decreases in anorexigenic Insulin is similar to leptin in the sense that both regulate body mass
pathways to promote food ingestion and restoration of energy ho- and/or food ingestion through negative feedback (45) and both have
meostasis (132,189) (Figure 2). been reported to decrease during periods of energy restriction (138).
It was with the discovery of leptin (211) and its relation with the fat Insulin acts in the brain as a potent anorexigenic hormone signaling
mass (FM) that a possible endocrine role on energy intake was eluci- “energy availability,” whereas peripherally lowers blood glucose
dated. We can take leptin, thyroid hormone, insulin, or ghrelin as levels, driving food intake (12,123). Insulin is also known for its
examples: Postprandial leptin levels have been shown to vary over the anticatabolic properties (171). This is relevant because, as Millward
course of weeks depending on adipose stores (69). These variations hypothesized (145), reductions in FFM have been shown to possess a
result in increased satiety after a meal (increased leptin levels/replete strong orexigenic effect (58) and are now being considered as a
adipose stores scenario) or decreased satiety (decreased leptin levels/ potent tonic appetite signal and a strong driver of food intake after
depleted adipose stores scenario), potentially regulating subsequential body mass loss (16,97). Ghrelin was discovered in 1999 (109) in the
food intake beyond the conscious control of an individual (137). stomach, whose main function is to regulate food intake and serve as
Leptin has also been shown to modulate hunger by other means such an orexigenic signal. Ghrelin levels have been shown to increase after
as inhibiting neuropeptide Y (NPY) and agouti-related protein (AgRP) diet-induced body mass loss (44) as well as upregulate during energy
neurons or stimulating proopiomelanocortin neurons in the hypo- restriction (18). It is thus commonly stated that these transient
thalamus (41,61). orexigenic signals in response to body mass loss can drive food
The thyroid gland hormones, particularly T3, are also of relevance consumption and increase appetite (207). Contrary to leptin, in-
when accounting for the EE of an individual (108). In a cohort of obese creases in ghrelin production underlie rises in AgRP and NPY neu-
children (168), reductions in T3 and T4 levels were observed after ropeptides, contributing to its orexigenic effect (5). Regarding
body mass losses in the long term, with no variation to thyroid stim- ghrelin, this study (117) reported how the response in circulating
ulating hormone. It is important to note that the levels of these hor- levels of ghrelin to meals with different calories was not equal be-
mones were altered at baseline among some of the subjects included in tween obese and lean subjects. Whereas ghrelin levels decreased after
the study (twofold above the SD for their age) and thus it could be high-calorie meals in the lean group and responsively increased after
debated if restoration of metabolic homeostasis through reductions in low-calorie meals (as expected), obese subjects didn’t exhibit
excessive FM was attributable for that outcome instead of body mass meaningful variations in ghrelin levels at all (117). This finding
loss per se. In another study of nonoverweight subjects (3), it was highlights how persistent endocrine alterations (obesity, in this case)
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Figure 2. Schematic representation of the endocrine control of energy balance. TDEE 5 total daily energy ex-
penditure; EAT 5 exercise-activity thermogenesis; REE/BMR 5 Resting energy expenditure/basal metabolic rate;
NEAT 5 non-exercise activity thermogenesis; TEF 5 Thermic effect of food; FM 5 fat mass; FFM 5 fat-free mass;
CCK 5 cholecystokinin; PYY 5 peptide YY; GLP-1 5 glucagon-like peptide 1. Adapted from various sources
(132,97,34,73,133).
can influence the outcomes of studies examining metabolic adapta- visually presents an integrative model of the endocrine regulation of
tion (163). Mechanisms for both leptin and ghrelin resistance in appetite and the feedback regulatory mechanisms that play a role in
obesity have been reported elsewhere (42,43). the dynamic nature of energy balance.
Other Hormones Involved in Physiological Adaptations to Nutritional Strategies to Reduce Metabolic

Body Mass Loss Adaptation to Body Mass Loss
Multiple additional alterations can be observed in the endocrine To determine the most adequate nutritional interventions to reduce
profile of other hormones related to appetite and satiety such as the deleterious effects of metabolic adaptation to body mass loss, we
gastric-inhibitory polypeptide (189) or amylin (169,189) with body must target the main issues responsible for this phenomenon, which
mass loss. Peptide YY (PYY) and cholecystokinin are gastrointestinal are increased hunger coupled with decreased EE (34,142,194).
GI peptides that can have an anorexigenic role regarding appetite Figure 4 summarizes the “energy gap concept,” which explains why
(205). Their production is sensitive to size, caloric content, and hunger and EE are the key drivers to design interventions to reduce
macronutrient composition of meals (187). Intervention studies in metabolic adaptation to body mass loss. High protein intakes, fiber,
obese humans report reductions in their respective circulating levels and intermittent energy restriction (IER) protocols (diet refeeds and
after a weight loss intervention (35,64,161), suggesting the notion breaks) have been proposed as nutritional strategies to have either a
that these hormones might play a role in weight regain. Glucagon- direct or a nondirect effect on sustained and successful body mass loss.
like peptide 1 (GLP-1) is secreted in the small intestine in response to Other factors such as increasing physical activity to maintain diet-
a nutrient load and has direct implications in the regulation of ap- induced body mass loss are of utmost importance to reduce our
petite (183). A study by De Luis et al. (49), which aimed to examine body’s compensatory responses (143), although this review will focus
the effect of body mass loss on GLP-1 levels, found a positive re- on the nutritional interventions.
lationship between the degree of body mass loss and reductions in
GLP-1. In a different study (1), similar results were observed, where
Rate of Body Mass Loss
GLP-1 levels decreased after body mass loss compared with baseline.
Thus, more research is warranted in this area. The speed at which body mass is lost has been thought to be of
To sum up the information displayed in this section; evidence has relevance when attempting to avoid metabolic adaptations and other
been presented to suggest that reductions in the circulating levels of undesirable outcomes while dieting. Although some evidence sug-
hormones that might possess an anorexigenic effect and increments in gests a steady approach to body mass loss (92,129), others appeal to
the ones whose role is mostly orexigenic have been reported in body the benefits of short-term approaches (10,153,166). On this premise,
mass loss intervention trials, both in the short term and long term. This it has been suggested that moderate-to-slow rates of body mass loss
might be reflective of our body’s attempt to restore energy homeo- would result in greater FM losses and less FFM and REE declines
stasis. We must not forget that samples pertaining to the available compared with faster rates of body mass loss (9). Consequences
studies are not always representative of the general population, let it be associated with rapid body mass loss might include the worsening of
the clinically obese or athletes. Thus, effect size and scientific relevance specific health biomarkers (182) while the improvement of others
of the findings cannot be always reliably assessed. The psychological, (154,195) or detrimental body composition changes in athletes (70).
behavioral, and environmental aspects regarding body mass loss and However, because most of these studies are performed in obese or
metabolic adaptation are out of the scope of this review; however, a overweight individuals, it could be argued whether any of the ben-
proper understanding and management of these variables is of high efits observed are because of the body mass loss rate or the absolute
relevance (130,175,191) to achieve successful body mass loss. Figure 3 body mass loss per se (113). In a recent comprehensive systematic
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Figure 3. A theoretical framework of metabolic adaptation. Note how increases in

hunger and slight reductions in TDEE after long periods of energy restriction exert
negative feedback on the initial deficit, attenuating the degree of weight loss.
Adapted from Trexler et al. (194). TDEE 5 total daily energy expenditure.
review on this topic (116), it was concluded that gradual rates of during periods of dietary restriction (32,33). To either maintain
weight loss were associated with greater losses in FM and body fat or increase LBM (a component of FFM), the rates of muscle
percentage as well as an enhanced maintenance of REE. The authors protein synthesis (MPS) must exceed muscle protein breakdown
highlighted the need for high quality studies with standardized in- (MPB) rates (148). A deeper understanding of protein turnover is
terventions as well as delimitations on what constitutes aggressive out of the scope of this review; the reader is redirected to other
and gradual energy restriction protocols to avoid heterogeneity reviews on the topic (94,164). Given the fact that protein might
(116). Besides, if potential body mass regain is a relevant outcome to possess a satiating effect (119,120) and has a higher thermic effect
measure, long-term high-quality trials are needed. after consumption (196), theory supports increasing protein in-
take over usual consumption patterns to mitigate potential in-
creases in hunger and appetite. In this trial with a randomized
Protein parallel design (201) in obese subjects who lost 5–10% of their
total body mass in 3 months, those who consumed 48 g of protein
One of the main contributors to the increase in appetite and
over their usual intake regained less body mass after the follow-up
hunger during energy restriction is thought to be FFM losses,
and mainly in the form of FFM. In another study (122), adding 30
which increases central signaling for food intake (58). Protein is
g·d21 of protein to the diet during 7 months resulted in less body
the most important macronutrient when accounting for the
mass regained in overweight subjects. To the author’s criteria,
maintenance of FFM and consequently for overall health during
lifespan (31,101) and our optimal needs might be increased both these studies were well conducted and showed no important
Figure 4. Visual representation of the energy gap concept. Lowering hunger and increasing
energy expenditure potentially narrows the difference between what is ingested and what is
expended, thus reducing the relative magnitude of the energy deficit, ensuring less metabolic
adaptation overall while still losing body mass. Adapted from Melby et al. (142). EAT 5
exercise activity thermogenesis; NEAT 5 non-EAT.
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limitations; however, it is important to note the studies were and they could improve the negative consequences of meta-
conducted by the same research group and although the results bolic adaptation.
may be extrapolated with ease, further replication of the findings
is warranted. In the DIOGENES study (4), a randomized con-
trolled trial performed in Europe with obese and overweight Carbohydrate and Fat
subjects on ad libitum diets, it was reported that after the initial
Outside protein, the carbohydrate-to-fat macronutrient compo-
body mass loss, those who consumed a higher amount of protein
sition of the diet has also been thought to play a role in potential
regained significantly less body mass than those with a lower
body mass regain after dieting. More precisely, the mathematical
intake. These results add up to the idea that increased protein

sum of the glycemic index (GI) (which is defined as the ability of a
might promote satiety and better body mass loss outcomes than a
specific food to rise glucose blood levels after a meal (103)) of the
usual intake—at least in the long term (121). Several meta-
foods in someone’s diet, also known as glycemic load (GL) (11),

analyses involving overweight and obese individuals suggest that
has received special attention due to the observed relationship
1.2–1.5 g·kg21 is an appropriate daily protein intake range to
between GI/GL and health outcomes (13,65).
maximize fat loss (107,112,208).
Acute spikes in insulin secretion as a result of adhering to a
Exercise also plays a relevant role in the maintenance of FFM
high-GL diet have been proposed to be one of the main re-
and the maintenance of EE during body mass loss. In a ran-
sponsible factors that would favor body mass regain while dieting
domized controlled trial by Verreijen et al. (198), 100 over-
through an increase of food cravings during the day, leading to
weight subjects on hypocaloric conditions underwent either a
overconsumption of calories. This partly conforms the “carbo-
10-week program with a high-protein (1.3 g·kg21) or a low-
hydrate-insulin” model of obesity (78). Although this model
protein diet (0.8 g·kg21) with or without resistance-type exer-
sounds great in theory, it falls in physiological reductionism and
cise. The results show how only the group with the combined
presents several flaws, as evidence to date fails to support it (78).
intervention (high protein and resistance exercise) preserved a
In this line of thought, a few interventions have aimed to compare
significant amount of FFM. After this idea, a recent meta-
low-carbohydrate (LC) diets (which are by definition low-GL
analysis (131) aimed to determine the effect of different types of
diets) to low-fat (LF) diets for body mass loss and body mass loss
exercise on EE, concluding that resistance exercise was slightly
maintenance (67,178). The overall results of these interventions
superior than endurance and aerobic exercise in increasing EE. It
show more pronounced body mass losses during the early phases
would also seem that in athletic populations, where the FFM
of the trial in the LC groups, which can be attributed to higher
component is generally larger than that of overweight and sed-
glycogen and water depletion rates (111), with attrition rates
entary individuals, protein needs during body mass loss might be
being high in both groups in the long term. In a randomized
even higher and of more relevance (106,162) ranging from 1.2
controlled trial by Ebbeling et al. (60), a LF diet, a low GI diet, and
to 2 g·kg21 of body mass. Mettler et al. (144) found a better
a LC diet were compared. After 10–15% body mass loss in
retention of LBM (skeletal muscle component of FFM) in indi-
overweight adults resulted in decreases in REE and TDEE in the
viduals who consumed 2.3 g of protein·kg21·d21 vs. those who
LF group but no decline was observed in the LC/low-GI groups.
consumed 1 g·kg21·d21 during a body mass loss protocol. In-
This study presents several limitations; First, diets were not
takes up to 3.4–4.4 g·kg21 have been studied before in this
equated for protein, so it could be argued that differences in the
population (6–8) with no deleterious health effects and im-
TEF (25) might have accounted for the differences observed in
provements in body composition reported.
TDEE between groups; Second, physical activity was reduced in
High-protein intakes should be recommended with caution
the LF diet group (TDEE to REE ratio) while it experimented an
because food choices to meet those goals may become difficult
increase in the LC respective to baseline levels (60). It has been
and adherence may be compromised. In studies that examined
previously reported how changes in spontaneous physical activity
very high intakes (6,7), daily protein requirements were ach-
account for significant variations in TDEE (38,126,141,199) so
ieved by supplementing with whey or beef protein. Dropout
this could help explain the results obtained. Overall, it seems that
rates from these studies were high (77 down to 48 and 40 down
the distribution of carbohydrate and fat is of little relevance when
to 30, respectively), and the reason given by the subjects was
designing a nutritional plan whose aim is to reduce metabolic
their inability to adhere to such high intakes, gastrointestinal
adaptation and prevent body mass regain. We must not forgo the
distress, or no reason at all. For a more personalized approach,
fact that most of these interventions were conducted in over-
it might be wise to estimate optimal protein needs based on
weight subjects. For athletes/leaner subjects, biasing energy intake
FFM or LBM (88,89,152) instead of total body mass because
toward carbohydrate while providing enough energy from fat
adipose tissue demands for protein are lower than those of
(10–25%) may help support exercise performance while on en-
FFM (36). However, because most people do not have access to
ergy restriction conditions (22,170,192).
accurate methods to determine FFM, adhering to the upper
range of recommendations (;2 g·kg21 of body mass) is ad-
vised for nonathletes with the goal of losing FM (101,106) with
even higher recommendations for those who aim to maximize
Fiber
hypertrophic adaptation (170). To conclude, increasing pro- The idea that dietary fiber might help control appetite is still
tein intake over usual values might be wise to offset the nega- controversial. As a public health strategy, it is indicated to in-
tives of dieting over long periods of time. It is important to crease fiber intake (98) because requirements are generally not
understand that recommended dietary allowances establish a met. Evidence from epidemiological studies reports higher-fiber
minimum, not an optimal intake (204) and thus should not be intakes to be associated with improved body mass control, higher
taken as a one-size-fits-all recommendation, especially during satiety, and overall lower-food intake (47,128,197). High-fiber
a caloric deficit. Combining high-protein intakes with a pre- foods generally possess a High satiety index (95). Possible ex-
scribed resistance exercise program seems to the best approach planatory mechanisms to this relation might reside in longer
to avoid FFM losses rather than increasing protein alone (149), chewing periods to consume high-fiber foods as well as its low-
2975
energy density (86,209). A meta-analysis (39) examined the re- control group with no advice to restrict calories for 1 year. No
lationship between acute satiety and consumption of fiber, find- significant differences were observed between the ICR and CER
ing no clear relationship between these 2 variables in group in regards to body mass loss and multiple other bio-
interventional studies. However, there is tremendous variability markers, concluding that both protocols were equally effective
in the design and methodology of fiber trials, where different in body mass reduction and disease prevention (179). In another
types of fiber may yield different outcomes (186). High-fiber trial on obese and overweight subjects (190), similar results were
meals can also modulate postprandial concentrations of an- observed; however, reported feelings of hunger were more
orexigenic gastrointestinal peptides such as GLP-1 and PYY common among the IER group after 1 year. One key aspect to
(115), thus contributing to increased satiety after a meal. Gastric consider when evaluating different dietary protocols is reported
emptying rate (GER) is also affected by fiber ingestion as dem- adherence (50,51). In both studies, the dropout rate from the
onstrated by Geliebter et al. (72). In their study, it was reported subjects was reported to be less than 10%, suggesting adherence
how oatmeal significantly lowered GER compared with corn to IER is similar to CER.
flakes (less fiber than oatmeal) and contributed to greater satiety Finally, athletes might benefit more from intermittent refeeds
after the meal. Different and varied fiber consumption might also than overweight subjects because this population has reported
contribute to a remodeling of the gut microbiota (93,134), which favorable results after this protocol (26). This might be due to
present numerous implications in the regulation of food intake carbohydrate being pertinent for sports performance outcomes
and overall health, yet further investigation is needed to make (21,82). Although not all kinds of sports may require high
conclusions. Overall, research on the satiating effects of fiber has amounts of carbohydrate to improve performance (37,63), they
been reported to present numerous methodological limitations are undoubtedly needed for high-intensity efforts (79,85). In a
and a lack of external validity (165). Randomized trials with very recent study by Campbell et al. (27), resistance-trained
subjects on hypocaloric conditions with high-fiber intakes subjects followed either 21% CER or 26% IER for 7 weeks.
through a whole-food approach are lacking. Thereby, designing Results showed similar reductions in body mass but higher re-
an approach toward increasing fiber to attenuate the effects of tention in dry FFM on the IER group. There are, nonetheless,
metabolic adaptation is complex. Because high-fiber intakes have several methodological considerations to address when inferring
been reported to reduce the energy density of the diet (59) as well conclusions from the evidence presented. Adherence was low (27
as allowing for larger volumes of food without drastically in- subjects completed the trial from the 58 who were instructed at
creasing calories (136), fiber could be a useful dietetic tool to baseline), the caloric restriction was different between groups (21
attain an energy deficit. vs 26%), and results were highly heterogeneous, with subjects
losing 3.5 kg of FFM and others gaining 2.5 kg within the IER
group (potentially due to the body assessment methods used).
Diet Refeeds and Diet Breaks This particular study caused a special interest in the community,
The current United States and European (104,210) guidelines with formal responses from both researchers in the field (160) and
recommend continuous energy restriction (CER) as an effective the main author of the study (28). Thus, conclusions should be
tool to lose body mass. On the other hand, IER includes a series of interpreted cautiously. Diet breaks are similar to refeeds but differ
nutritional protocols that differ from the traditional approach of in the amount of time where energy balance conditions are met
dieting in CER (159,177), in the sense that they alternate periods (from 1 to 2 days up to weeks). Because metabolic adaptations
of overfeeding with periods of undereating, which still follow the have been shown to persist even after years after initial body mass
principles of energy balance (76). The most common IER proto- loss (189), diet breaks are used on the premise that compensatory
cols used are diet breaks and refeeds. Diet refeeds could be defined responses to body mass loss require longer periods in energy
as a specific dietetic strategy where calories and macronutrients balance conditions to partially or completely return to baseline
are increased at energy maintenance levels or slightly above on (23,90).
specific days (1–2 days) over the course of a weekly deficit, pre- Evidence for the use of diet breaks is also mixed. In the
dominantly achieved by increasing carbohydrate consumption MATADOR study (24), 51 obese subjects followed CER or IER
(62,194). alternating weeks of energy balance (14 weeks) with periods of
There are several hypotheses to why increasing carbohydrate energy restriction (16 weeks) during a total of 30 weeks. The
periodically could lead to improved body mass loss outcomes results reported greater body mass loss among the subjects of the
and better FFM retention; First, because circulating insulin IER compared with the CER group, as other studies have also
levels have a role in the maintenance of FFM (171) responses in replicated (48). By contrast, another study (203) found no dif-
secretion to acute carbohydrate refeeds could help reduce MPB ference between diet break protocols over traditional caloric re-
(15,75) as well as promote a more pronounced MPS response striction after 14 weeks. An important consideration regarding
through the activation of the mTORC1 pathway (200). Second, the methodology of the previous study is that the CER group
leptin has been demonstrated to be especially responsive to performed a 2-week break (was not strictly continuous), whereas
carbohydrate intake (102). To test if overfeeding alone was the IER group followed a 6-week diet break. Because it is not well
solely responsible for the rise in leptin, a study (52) was con- understood how much time of a break is needed to revert the
ducted on lean healthy female subjects aimed to compare fat vs. compensatory adaptations to body mass loss (176), this factor
carbohydrate refeeds. Plasma leptin levels were elevated after a could have played in favor of the CER group, thus resembling the
carbohydrate overfeed but not a fat overfeed, suggesting car- outcome. Peos et al. (158) will examine the effect of IER strategies
bohydrate to have a major impact on leptin levels. Overweight in the medium-to-long term in the ICECAP trial that is currently
and obese subjects may benefit from this strategy because a se- in the works whose results are expected to be released soon. To
ries of hormonal alterations such as leptin resistance have been forge a more solid answer to the question, recent meta-analyses
reported in this population (81). In another study (179), obese (80,83,84) examined the effects of IER to CER in regards to body
and overweight subjects were randomly allocated in either an mass loss, concluding that there was no significant difference
IER group with refeeding every 5 days, a CER group, or a between both protocols. It was also reported how the number of
2976
studies included was small and presented huge heterogeneity. In 13. Barclay AW, Petocz P, McMillan-Price J, et al. Glycemic index, glycemic
addition, most of them were at an unclear risk of bias, and most load, and chronic disease risk—A metaanalysis of observational studies.
Am J Clin Nutr 87: 627–637, 2008.
differences in secondary outcomes such as insulin sensitivity and 14. Bevilacqua L, Ramsey JJ, Hagopian K, Weindruch R, Harper ME. Effects
other biomarkers could be solely attributed to body mass loss of short- and medium-term calorie restriction on muscle mitochondrial
itself. proton leak and reactive oxygen species production. Am J Physiol
Endocrinol Metab 286: E852–E861, 2004.
15. Bird SP, Tarpenning KM, Marino FE. Independent and combined effects
of liquid carbohydrate/essential amino acid ingestion on hormonal and
Practical Applications muscular adaptations following resistance training in untrained men.
Eur J Appl Physiol 97: 225–238, 2006.

Changes in EE during body mass loss occur, but are largely 16. Blundell JE, Caudwell P, Gibbons C, et al. Role of resting metabolic rate
explained by involuntary changes in the non-exercise activity and energy expenditure in hunger and appetite control: A new formu-
compartment (NEAT). Alongside changes in EE, endocrine lation. DMM Dis Models Mech 5: 608–613, 2012.
and physiological alterations occurs to increase appetite, 17. Bray GA, Redman LM, De Jonge L, et al. Effect of protein overfeeding on
energy expenditure measured in a metabolic chamber. Am J Clin Nutr
which represents the homeostatic drive to restore lost weight. 101: 496–505, 2015.
High-protein diets ranging from 1.2 to 1.5 g.kg-1 in over- 18. Briggs DI, Andrews ZB. Metabolic status regulates ghrelin function on
weight individuals and up to 2 g.kg-1 are effective in lean energy homeostasis. Neuroendocrinology 93: 48–57, 2011.
athletes to preserve FFM. High-fiber foods, such as whole 19. Broeders EPM, Vijgen GHEJ, Havekes B, et al. Thyroid hormone acti-
vates Brown adipose tissue and increases non-shivering
grains, fruits, and vegetables, are also recommended because thermogenesis—A cohort study in a group of thyroid carcinoma pa-
they generate early satiation and allow for large volumes of tients. PLoS One 11: e0145049, 2016.
food to be consumed while dieting. Concerning diet refeeds 20. Browning MG. Methodologic considerations in the evaluation of
and diet breaks, the evidence is mixed and scarce. However, adaptive thermogenesis. Am J Clin Nutr 103: 952–953, 2016.
some positive results for IER have been reported in certain 21. Burke LM, Hawley JA, Jeukendrup A, et al. Toward a common un-
derstanding of diet-exercise strategies to manipulate fuel availability for
scenarios (24,27) where both athletes and overweight subjects training and competition preparation in endurance sport. Int J Sport
might benefit from it as a part of a periodized body mass loss Nutr Exerc Metab 28: 451–463, 2018.
program. Nondietary interventions, such as increasing phys- 22. Burke LM, Castell LM, Casa DJ, et al. International Association of
ical activity EE and engaging in programmed resistance Athletics Federations consensus statement 2019: Nutrition for athletics.
Int J Sport Nutr Exerc Metab 29: 73–84, 2019.
training, are also advised as they minimize the deleterious ef- 23. Byrne NM, Hills AP. Biology or behavior: Which is the strongest con-
fects of metabolic adaptation to body mass loss. tributor to weight gain? Curr Obes Rep 2: 65–76, 2013.
24. Byrne NM, Sainsbury A, King NA, Hills AP, Wood RE. Intermittent
energy restriction improves weight loss efficiency in obese men: The
MATADOR study. Int J Obes 42: 129–138, 2018.
References 25. Calcagno M, Kahleova H, Alwarith J, et al. The thermic effect of food: A
1. Adam TCM, Jochan J, Westerterp-Plantenga MS. Decreased glucagon- review. J Am Coll Nutr 38: 547–551, 2019.
like peptide 1 release after weight loss in overweight/obese subjects. Obes 26. Campbell B, Aguilar D, Wong V, et al. The effects of intermittent car-
Res 13: 710–716, 2005. bohydrate re-feeds vs. continuous dieting on resting metabolic rate in
2. Adriaens MPE, Schoffelen PFM, Westerterp KR. Intra-individual varia- resistance trained individuals: A flexible dieting study. Proceedings of the
tion of basal metabolic rate and the influence of daily habitual physical Fifteenth International Society of Sports Nutrition (ISSN) Conference
activity before testing. Br J Nutr 90: 419–423, 2003. and Expo. J Int Soc Sports Nutr 15: 1–37, 2018.
3. Agnihothri RV, Courville AB, Linderman JD, et al. Moderate weight loss 27. Campbell BI, Aguilar D, Colenso-semple LM, et al. Intermittent energy
is sufficient to affect thyroid hormone homeostasis and inhibit its pe- restriction attenuates the loss of fat free mass in resistance trained indi-
ripheral conversion. Thyroid 24: 19–26, 2014. viduals: A randomized controlled trial. J Funct Morphol Kinesiol 5: 19,
4. Aller EEJG, Larsen TM, Claus H, et al. Weight loss maintenance in 2020.
overweight subjects on ad libitum diets with high or low protein content 28. Campbell BI. A reply to contrary to the conclusions stated in the paper,
and glycemic index: The DIOGENES trial 12-month results. Int J Obes only dry fat-free mass was different between groups upon reanalysis—
38: 1511–1517, 2014. Comment on: “Intermittent energy restriction attenuates the loss of fat-
5. Andrews ZB, Liu ZW, Walllingford N, et al. UCP2 mediates ghrelin’s free mass in resistance trained individuals: A randomized controlled
action on NPY/AgRP neurons by lowering free radicals. Nature 454: trial”. J Funct Morphol Kinesiol 5: 86, 2020.
846–851, 2008. 29. Cannon B, Nedergaard J. Brown adipose tissue: Function and physio-
6. Antonio J, Peacock CA, Ellerbroek A, Fromhoff B, Silver T. The effects of logical significance. Physiol Rev 81: 277–359, 2004.
consuming a high protein diet (4.4 g/kg/d) on body composition in 30. Cannon B, Nedergaard J. Thermogenesis challenges the adipostat
resistance-trained individuals. J Int Soc Sports Nutr 11: 1–6, 2014. hypothesis for body-weight control. Proc Nutr Soc 68: 401–407,
7. Antonio J, Ellerbroek A, Silver T, et al. A high protein diet (3.4 g/kg/d) 2009.
combined with a heavy resistance training program improves body 31. Carbone JW, Pasiakos SM. Dietary protein and muscle mass: Translating
composition in healthy trained men and women - a follow-up in- science to application and health benefit. Nutrients 11: 1–13, 2019.
vestigation. J Int Soc Sports Nutr 12: 39, 2015. 32. Carbone JW, McClung JP, Pasiakos SM. Skeletal muscle responses to
8. Antonio J, Ellerbroek A, Silver T, Vargas L, Peacock C. The effects of a negative energy balance: Effects of dietary protein. Adv Nutr 3: 119–126,
high protein diet on indices of health and body composition—A cross- 2012.
over trial in resistance-trained men. J Int Soc Sports Nutr 13: 3, 2016. 33. Carbone JW, McClung JP, Pasiakos SM. Recent advances in the char-
9. Ashtary-Larky D, Ghanavati M, Lamuchi-Deli N, et al. Rapid weight acterization of skeletal muscle and whole-body protein responses to di-
loss vs. slow weight loss: Which is more effective on body composition etary protein and exercise during negative energy balance. Adv Nutr 10:
and metabolic risk factors? Int J Endocrinol Metab 15: e13249, 2017. 70–79, 2019.
10. Astrup A, Rössner S. Lessons from obesity management programmes: 34. Casanova N, Beaulieu K, Finlayson G, Hopkins M. Metabolic adapta-
Greater initial weight loss improves long-term maintenance. Obes Rev 1: tions during negative energy balance and their potential impact on ap-
17–19, 2000. petite and food intake. Proc Nutr Soc 78: 279–289, 2019.
11. Augustin LSA, Kendall CWC, Jenkins DJA, et al. Glycemic index, gly- 35. Chearskul S, Delbridge E, Shulkes A, Proietto J, Kriketos A. Effect of
cemic load and glycemic response: An International Scientific Consensus weight loss and ketosis on postprandial cholecystokinin and free fatty
Summit from the International Carbohydrate Quality Consortium acid concentrations. Am J Clin Nutr 87: 1238–1246, 2008.
(ICQC). Nutr Metab Cardiovasc Dis 25: 795–815, 2015. 36. Choe SS, Huh JY, Hwang IJ, Kim JI, Kim JB. Adipose tissue remodeling:
12. Austin J, Marks D. Hormonal regulators of appetite. Int J Pediatr Its role in energy metabolism and metabolic disorders. Front Endocrinol
Endocrinol 1: 1–9, 2009. 7: 30, 2016.
2977
37. Cholewa JM, Newmire DE, Zanchi NE. Carbohydrate restriction: 62. Escalante G, Campbell BI, Norton L. Effectiveness of diet refeeds and diet
Friend or foe of resistance-based exercise performance? Nutr 60: breaks as a precontest strategy. Strength Cond J: 1, 2020.
136–146, 2019. 63. Escobar KA, Vandusseldorp TA, Kerksick CM. Carbohydrate intake
38. Chung N, Park MY, Kim J, et al. Non-exercise activity thermogenesis and resistance-based exercise: Are current recommendations reflective of
(NEAT): A component of total daily energy expenditure. J Exerc Nutr actual need? Br J Nutr 116: 2053–2065, 2016.
Biochem 22: 23, 2018. 64. Essah PA, Levy JR, Sistrun SN, Kelly SM, Nestler JE. Effect of weight loss
39. Clark MJ, Slavin JL. The effect of fiber on satiety and food intake: A by a low-fat diet and a low-carbohydrate diet on peptide YY levels. Int J
systematic review. J Am Coll Nutr 32: 200–211, 2013. Obes 34: 1239–1242, 2010.
40. Cowley MA, Pronchuk N, Fan W, et al. Integration of npy, agrp, 65. Fan J, Song Y, Wang Y, Hui R, Zhang W. Dietary glycemic index, gly-
and melanocortin signals in the hypothalamic paraventricular nu- cemic load, and risk of coronary heart disease, stroke, and stroke mor-
cleus: Evidence of a cellular basis for the adipostat. Neuron 24: tality: A systematic review with meta-analysis. PLoS One 7: e52182,
155–163, 1999. 2012.
41. Cowley MA, Smart JL, Rubinstein M, et al. Leptin activates anorexigenic 66. Fine EJ, Feinman RD. Thermodynamics of weight loss diets. Nutr Metab
POMC neurons through a neural network in the arcuate nucleus. Nature 1: 1–8, 2004.
411: 480–484, 2001. 67. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-
42. Crujeiras AB, Goyenechea E, Abete I, et al. Weight regain after a diet- carbohydrate diet for obesity. N Engl J Med 348: 2082–2090, 2003.
induced loss is predicted by higher baseline leptin and lower ghrelin 68. Freire R. Scientific evidence of diets for weight loss: Different macronu-
plasma levels. J Clin Endocrinol Metab 95: 5037–5044, 2010. trient composition, intermittent fasting, and popular diets. Nutrition 69:
43. Cui H, L ópez M, Rahmouni K. The cellular and molecular bases of 110549, 2020.
leptin and ghrelin resistance in obesity. Nat Rev Endocrinol 13: 338, 69. Friedman JM. Leptin and the endocrine control of energy balance. Nat
2017. Metab 1: 754–764, 2019.
44. Cummings DE, Weigle DS, Scott Frayo R, et al. Plasma ghrelin levels 70. Garthe I, Raastad T, Refsnes PE, Koivisto A, Sundgot-Borgen J. Effect of
after diet-induced weight loss or gastric bypass surgery. N Engl J Med two different weight-loss rates on body composition and strength and
346: 1623–1630, 2002. power-related performance in elite athletes. Int J Sport Nutr Exerc Metab
45. Cummings DE, Overduin J, Foster-Schubert KE. Roles for ghrelin in the 21: 97–104, 2011.
regulation of appetite and body weight. Curr Opin Endocrinol Diabetes 71. Geisler CE, Hepler C, Higgins MR, Renquist BJ. Hepatic adaptations to
138: 389–396, 2005. maintain metabolic homeostasis in response to fasting and refeeding in
46. Curtis V, Henry CJK, Birch E, Ghusain-Choueiri A. Intraindividual mice. Nutr Metab 13: 62, 2016.
variation in the basal metabolic rate of women: Effect of the menstrual 72. Geliebter A, Grillot CL, Aviram-Friedman R, et al. Effects of oatmeal and
cycle. Am J Hum Biol 8: 631–639, 1996. corn flakes cereal breakfasts on satiety, gastric emptying, glucose, and
47. Davis JN, Hodges VA, Gillham MB. Normal-weight adults consume appetite-related hormones. Ann Nutr Metab 66: 93–103, 2015.
more fiber and fruit than their age- and height-matched overweight/obese 73. Greenway FL. Physiological adaptations to weight loss and factors
counterparts. J Am Diet Assoc 106: 833–840, 2006. favouring weight regain. Int J Obes 39: 1188–1196, 2015.
48. Davoodi SH, Ajami M, Ayatollahi SA, et al. Calorie shifting diet versus 74. Guo J, Hall KD. Predicting changes of body weight, body fat, energy
calorie restriction diet: A comparative clinical trial study. Int J Prev Med expenditure and metabolic fuel selection in C57BL/6 mice. PLoS One 6:
5: 447, 2014. e15961, 2011.
49. De Luis DA, Gonzalez Sagrado M, Conde R, Aller R, Izaola O. De- 75. Halberg N, Henriksen M, Söderhamn N, et al. Effect of intermittent
creased basal levels of glucagon-like peptide-1 after weight loss in obese fasting and refeeding on insulin action in healthy men. J Appl Physiol
subjects. Ann Nutr Metab 51: 134–138, 2007. (1985) 99: 2128–2136, 2005.
50. Del Corral P, Bryan DR, Garvey WT, Gower BA, Hunter GR. Dietary 76. Hall KD, Heymsfield SB, Kemnitz JW, et al. Energy balance and its
adherence during weight loss predicts weight regain. Obesity 19: components: Implications for body weight regulation. Am J Clin Nutr
1177–1181, 2011. 95: 989–994, 2012.
51. Desroches S, Lapointe A, Ratté S, et al. Interventions to enhance ad- 77. Hall KD. Predicting metabolic adaptation, body weight change, and
herence to dietary advice for preventing and managing chronic diseases energy intake in humans. Am J Physiol Endocrinol Metab 298:
in adults. Cochrane Database Syst Rev CD008722, 2013. E449–E466, 2010.
52. Dirlewanger M, Di Vetta V, Guenat E, et al. Effects of short-term car- 78. Hall KD. A review of the carbohydrate-insulin model of obesity. Eur J
bohydrate or fat overfeeding on energy expenditure and plasma leptin Clin Nutr 71: 323–326, 2017.
concentrations in healthy female subjects. Int J Obes 24: 1413–1418, 79. Hargreaves M, Spriet LL. Exercise metabolism: Fuels for the fire. Cold
2000. Spring Harb Perspect Med 8: 1–16, 2018.
53. Donahoo WT, Levine JA, Melanson EL. Variability in energy expendi- 80. Harris L, McGarty A, Hutchison L, Ells L, Hankey C. Short-term in-
ture and its components. Curr Opin Clin Nutr Metab Care 7: 599–605, termittent energy restriction interventions for weight management: A
2004. systematic review and meta-analysis. Obes Rev 19: 1–13, 2018.
54. Doucet E, Imbeault P, St-Pierre S, et al. Greater than predicted decrease in 81. Havel PJ. Role of adipose tissue in body-weight regulation: Mechanisms
energy expenditure during exercise after body weight loss in obese men. regulating leptin production and energy balance. Proc Nutr Soc 59:
Clin Sci 105: 89–95, 2003. 359–371, 2000.
55. Dulloo AG, Jacquet J, Girardier L. Poststarvation hyperphagia and body 82. Hawley JA, Schabort EJ, Noakes TD, Dennis SC. Carbohydrate-loading
fat overshooting in humans: A role for feedback signals from lean and fat and exercise performance. Sports Med 24: 73–81, 1997.
tissues. Am J Clin Nutr 65: 717–723, 1997. 83. He S, Wang J, Zhang J, Xu J. Intermittent versus continuous energy
56. Dulloo AG, Jacquet J, Montani JP, Schutz Y. Adaptive thermogenesis in restriction for weight loss and metabolic improvement: A meta-analysis
human body weight regulation: More of a concept than a measurable and systematic review. Obesity 29: 108–115, 2021.
entity? Obes Rev 13: 105–121, 2012. 84. Headland M, Clifton PM, Carter S, Keogh JB. Weight-loss outcomes: A
57. Dulloo AG, Jacquet J, Montani JP. How dieting makes some fatter: From systematic review and meta-analysis of intermittent energy restriction
a perspective of human body composition autoregulation. Proc Nutr Soc trials lasting a minimum of 6 months. Nutrients 8: 354, 2016.
71: 379–389, 2012. 85. Hearris MA, Hammond KM, Fell JM, Morton JP. Regulation of muscle
58. Dulloo AG, Miles-Chan JL, Schutz Y. Collateral fattening in body glycogen metabolism during exercise: Implications for endurance per-
composition autoregulation: Its determinants and significance for obe- formance and training adaptations. Nutrients 10: 1–21, 2018.
sity predisposition. Eur J Clin Nutr 72: 657–664, 2018. 86. Heaton KW, Haber GB, Burroughs L, Murphy D. How fiber may pre-
59. Duncan KH, Bacon JA, Weinsier RL. The effects of high and low energy vent obesity: Promotion of satiety and prevention of rebound hypogly-
density diets on satiety, energy intake, and eating time of obese and cemia. Am J Clin Nutr 31: S280, 1978.
nonobese subjects. Am J Clin Nutr 37: 763–767, 1983. 87. Hector AJ, McGlory C, Damas F, et al. Pronounced energy restriction
60. Ebbeling CB, Swain JF, Feldman HA, et al. Effects of dietary composition with elevated protein intake results in no change in proteolysis and re-
on energy expenditure during weight-loss maintenance. JAMA 307: ductions in skeletal muscle protein synthesis that are mitigated by re-
2627–2634, 2012. sistance exercise. FASEB J 32: 265–275, 2018.
61. Elias CF, Aschkenasi C, Lee C, et al. Leptin differentially regulates NPY 88. Helms ER, Aragon AA, Fitschen PJ. Evidence-based recommendations
and POMC neurons projecting to the lateral hypothalamic area. Neuron for natural bodybuilding contest preparation: Nutrition and supple-
23: 775–786, 1999. mentation. J Int Soc Sports Nutr 11: 1–20, 2014.
2978
89. Helms ER, Zinn C, Rowlands DS, Brown SR. A systematic review of 115. Lafond DW, Greaves KA, Maki KC, Leidy HJ, Romsos DR. Effects of
dietary protein during caloric restriction in resistance trained lean ath- two dietary fibers as part of ready-to-eat cereal (RTEC) breakfasts on
letes: A case for higher intakes. Int J Sport Nutr Exerc Metab 24: perceived appetite and gut hormones in overweight women. Nutrients 7:
127–138, 2014. 1245–1266, 2015.
90. Henry RR, Scheaffer L, Olefsky JM. Glycemic effects of intensive caloric 116. Larky DA, Bagheri R, Abbasnezhad A, et al. Effects of gradual weight
restriction and isocaloric refeeding in noninsulin-dependent diabetes loss vs rapid weight loss on body composition and resting metabolic rate:
mellitus. J Clin Endocrinol Metab 61: 917–925, 1985. A systematic review and meta-analysis. Br J Nutr: 1–26, 2020.
91. Henry CJK. Mechanisms of changes in basal metabolism during ageing. 117. Le Roux CW, Patterson M, Vincent RP, et al. Postprandial plasma
Eur J Clin Nutr 54: S77–S91, 2000. ghrelin is suppressed proportional to meal calorie content in normal-
92. Hill JO. Can a small-changes approach help address the obesity epi- weight but not obese subjects. J Clin Endocrinol Metab 90: 1068–1071,
demic? A report of the Joint Task Force of the American Society for 2005.
Nutrition, Institute of Food Technologists, and International Food In- 118. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure
formation Council. Am J Clin Nutr 89: 477–484, 2009. resulting from altered body weight. N Engl J Med 332: 621–628,
93. Hills RD, Pontefract BA, Mishcon HR, et al. Gut microbiome: Profound 1995.
implications for diet and disease. Nutrients 11: 1–40, 2019. 119. Leidy HJ, Mattes RD, Campbell WW. Effects of acute and chronic
94. Hinkson IV, Elias JE. The dynamic state of protein turnover: It’s about protein intake on metabolism, appetite, and ghrelin during weight loss.
time. Trends Cell Biol 21: 293–303, 2011. Obesity 15: 1215–1225, 2007.
95. Holt SHA, Brand Miller JC, Petocz P, Farmakalidis E. A satiety index of 120. Leidy HJ, Tang M, Armstrong CLH, Martin CB, Campbell WW. The
common foods. Eur J Clin Nutr 49: 675–690, 1995. effects of consuming frequent, higher protein meals on appetite and sa-
96. Hopkins M, Blundell JE. Energy balance, body composition, sedentari- tiety during weight loss in overweight/obese men. Obesity 19: 818–824,
ness and appetite regulation: Pathways to obesity. Clin Sci 130: 2011.
1615–1628, 2016. 121. Leidy HJ, Clifton PM, Astrup A, et al. The role of protein in weight loss
97. Hopkins M, Beaulieu K, Myers A, Gibbons C, Blundell JE. Mechanisms and maintenance. Am J Clin Nutr 101: 1320S–1329S, 2015.
responsible for homeostatic appetite control: Theoretical advances and 122. Lejeune MPGM, Kovacs EMR, Westerterp-Plantenga MS. Additional
practical implications. Expert Rev Endocrinol Metab 12: 401–415, protein intake limits weight regain after weight loss in humans. Br J Nutr
2017. 93: 281–289, 2005.
98. Howarth NC, Saltzman E, Roberts SB. Dietary fiber and weight regu- 123. Lenard NR, Berthoud HR. Central and peripheral regulation of food
lation. Nutr Rev 59: 129–139, 2009. intake and physical activity: Pathways and genes. Obesity 16: S11–S22,
99. Hulmi JJ, Isola V, Suonpää M, et al. The effects of intensive weight 2008.
reduction on body composition and serum hormones in female fitness 124. Levine JA, Vander Weg MW, Hill JO, Klesges RC. Non-exercise activity
competitors. Front Physiol 7: 689, 2017. thermogenesis: The crouching tiger hidden dragon of societal weight
100. Intake SF, Loss W, Bellissimo N, Akhavan T. Effect of macronutrient gain. Arterioscler Thromb Vasc Biol 26: 729–736, 2006.
composition on short-term food intake and weight loss. Adv Nutr 6: 125. Levine JA, Eberhardt NL, Jensen MD. Role of nonexercise activity
302–308, 2015. thermogenesis in resistance to fat gain in humans. Science 283: 212–214,
101. Jäger R, Kerksick CM, Campbell BI, et al. International Society of Sports 1999.
Nutrition position stand Protein and exercise. J Int Soc Sports Nutr 14: 126. Levine JA. Non-exercise activity thermogenesis (NEAT). Best Pract Res
1–25, 2017. Clin Endocrinol Metab 16: 679–702, 2002.
102. Jenkins AB, Markovic TP, Fleury A, Campbell LV. Carbohydrate intake 127. Levine JA. Measurement of energy expenditure. Public Health Nutr 8:
and short-term regulation of leptin in humans. Diabetologia 40: 1123–1132, 2005.
348–351, 1997. 128. Liu S, Willett WC, Manson JAE, et al. Relation between changes in
103. Jenkins DJA, Kendall CWC, Augustin LSA, et al. Glycemic index: intakes of dietary fiber and grain products and changes in weight and
Overview of implications in health and disease. Am J Clin Nutr 76: development of obesity among middle-aged women. Am J Clin Nutr 78:
266S–273S, 2002. 920–927, 2003.
104. Jensen MD, Ryan DH, Donato KA, et al. Executive summary: Guidelines 129. Lutes L, Wientt R, Barger S, et al. Small changes in nutrition and physical
(2013) for the management of overweight and obesity in adults. Obesity activity promote weight loss and maintenance: 3-month evidence from
22: S5–S39, 2014. the ASPIRE randomized trial. Ann Behav Med 35: 351–357, 2008.
105. Kennedy GC. The role of depot fat in the hypothalamic control of food 130. Lytle LA, Nicastro HL, Roberts SB, et al. Accumulating data to optimally
intake in the rat. Proc R Soc Lond Ser B, Biol Sci 140: 578–592, 1953. predict obesity treatment (ADOPT) core measures: Behavioral domain.
106. Kerksick CM, Wilborn CD, Roberts MD, et al. ISSN exercise & sports Obesity 26: S16–S24, 2018.
nutrition review update: Research & recommendations. J Int Soc Sports 131. MacKenzie-Shalders K, Kelly JT, So D, Coffey VG, Byrne NM. The effect
Nutr 15: 1–57, 2018. of exercise interventions on resting metabolic rate: A systematic review
107. Kim JE, O’Connor LE, Sands LP, Slebodnik MB, Campbell WW. Effects and meta-analysis. J Sports Sci 8: 1635–1649, 2020.
of dietary protein intake on body composition changes after weight loss 132. MacLean PS, Bergouignan A, Cornier MA, Jackman MR. Biology’s re-
in older adults: A systematic review and meta-analysis. Nutr Rev 74: sponse to dieting: The impetus for weight regain. Am J Physiol Regul
210–224, 2016. Integr Comp Physiol 301: R581–600, 2011.
108. Kim B. Thyroid hormone as a determinant of energy expenditure and the 133. MacLean PS, Blundell JE, Mennella JA, Batterham RL. Biological con-
basal metabolic rate. Thyroid 18: 141–144, 2008. trol of appetite: A daunting complexity. Obesity 25(Suppl 1): S8–S16,
109. Kojima M, Hosoda H, Date Y, et al. Ghrelin is a growth-hormone- 2017.
releasing acylated peptide from stomach. Nature 402: 656–660, 1999. 134. Makki K, Deehan EC, Walter J, Bäckhed F. The impact of dietary fiber
110. Konturek SJ, Konturek JW, Pawlik T, Brzozowki T. Brain-gut axis and on gut microbiota in host health and disease. Cell Host Microbe 23:
its role in the control of food intake. J Physiol Pharmacol 55: 137–154, 705–715, 2018.
2004. 135. Malik VS, Hu FB. Popular weight-loss diets: From evidence to practice.
111. Kreitzman SN, Coxon AY, Szaz KF. Glycogen storage: Illusions of easy Nat Clin Pract Cardiovasc Med 4: 34–41, 2007.
weight loss, excessive weight regain, and distortions in estimates of body 136. Manore MM. Weight management for athletes and active individuals: A
composition. Am J Clin Nutr 56: 292S–293S, 1992. brief review. Sports Med 45: 83–92, 2015.
112. Krieger JW, Sitren HS, Daniels MJ, Langkamp-Henken B. Effects of 137. Margetic S, Gazzola C, Pegg GG, Hill RA. Leptin: A review of its
variation in protein and carbohydrate intake on body mass and com- peripheral actions and interactions. Int J Obes 26: 1407–1433,
position during energy restriction: A meta-regression 1. Am J Clin Nutr 2002.
83: 260–274, 2006. 138. Mars M, De Graaf C, De Groot LCPGM, Kok FJ. Decreases in fasting
113. Kuk JL, Christensen RAG, Wharton S. Absolute weight loss, and not leptin and insulin concentrations after acute energy restriction and sub-
weight loss rate, is associated with better improvements in metabolic sequent compensation in food intake. Am J Clin Nutr 81: 570–577,
health. J Obes 2019: 3609642, 2019. 2005.
114. La Bounty PM, Campbell BI, Wilson J, et al. International Society of 139. Martins C, Gower BA, Hill JO, Hunter GR. Metabolic adaptation is not
Sports Nutrition position stand: Meal frequency. J Int Soc Sports Nutr 8: a major barrier to weight-loss maintenance. Am J Clin Nutr 558–565,
1–12, 2011. 2020.
2979
140. Martins C, Roekenes J, Salamati S, Gower BA, Hunter GR. Metabolic 165. Poutanen KS, Dussort P, Erkner A, et al. A review of the characteristics of
adaptation is an illusion, only present when participants are in negative dietary fibers relevant to appetite and energy intake outcomes in human
energy balance. Am J Clin Nutr 112: 1212–1218, 2020. intervention trials. Am J Clin Nutr 106: 747–754, 2017.
141. McClave SA, Snider HL. Dissecting the energy needs of the body. Curr 166. Purcell K, Sumithran P, Prendergast LA, et al. The effect of rate of weight
Opin Clin Nutr Metab Care 4: 143–147, 2001. loss on long-term weight management: A randomised controlled trial.
142. Melby CL, Paris HL, Foright RM, Peth J. Attenuating the biologic drive Lancet Diabetes Endocrinol 2: 954–962, 2014.
for weight regain following weight loss: Must what goes down always go 167. Quatela A, Callister R, Patterson A, Macdonald-Wicks L. The energy
back up? Nutrients 9: 468, 2017. content and composition of meals consumed after an overnight fast and
143. Melby CL, Paris HL, Drew Sayer R, Bell C, Hill JO. Increasing energy their effects on diet induced thermogenesis: A systematic review, meta-
flux to maintain diet-induced weight loss. Nutrients 11: 2533, 2019. analyses and meta-regressions. Nutrients 8: 670, 2016.
144. Mettler S, Mitchell N, Tipton KD. Increased protein intake reduces lean 168. Reinehr T, Andler W. Thyroid hormones before and after weight loss in
body mass loss during weight loss in athletes. Med Sci Sports Exerc 42: obesity. Arch Dis Child 87: 320–323, 2002.
326–337, 2010. 169. Reinehr T, De Sousa G, Niklowitz P, Roth CL. Amylin and its relation to
145. Millward DJ. A protein-stat mechanism for regulation of growth and insulin and lipids in obese children before and after weight loss. Obesity
maintenance of the lean body mass. Nutr Res Rev 8: 93–120, 1995. 15: 2006–2011, 2007.
146. Miles WR, et al. Review of the biology of human starvation [Review of 170. Roberts BM, Helms ER, Trexler ET, Fitschen PJ. Nutritional recom-
the book “The Biology of Human Starvation”, by A. Keys, J. Brozek, A. mendations for physique athletes. J Hum Kinet 71: 79–108, 2020.
Henschel, O. Mickelsen, H. L. Taylor, E. Simonson, A. S. Skinner & S. 171. Rooyackers OE, Nair KS. Hormonal regulation OF human muscle
M. Wells]. J Abnorm Soc Psychol 47: 735–739, 1952. protein metabolism. Annu Rev Nutr 17: 457–485, 1997.
147. Moehlecke M, Canani LH, e Silva LOJ, et al. Determinants of body 172. Rosenbaum M, Leibel RL. Adaptive thermogenesis in humans. Int J
weight regulation in humans. Arch Endocrinol Metab 60: 152–162, Obes 34: S47–S55, 2010.
2016. 173. Rosenbaum M, Leibel RL. Models of energy homeostasis in response to
148. Moore DR. Maximizing post-exercise anabolism: The case for relative maintenance of reduced body weight. Obesity 24: 1620–1629, 2016.
protein intakes. Front Nutr 6: 1–13, 2019. 174. Rossow LM, Fukuda DH, Fahs CA, Loenneke JP, Stout JR. Natural
149. Morton RW, Murphy KT, McKellar SR, et al. A systematic review, meta- bodybuilding competition preparation and recovery: A 12-month case
analysis and meta-regression of the effect of protein supplementation on study. Int J Sports Physiol Perform 8: 582–592, 2013.
resistance training-induced gains in muscle mass and strength in healthy 175. Saelens BE, Arteaga SS, Berrigan D, et al. Accumulating data to optimally
adults. Br J Sports Med 52: 376–384, 2018. predict obesity treatment (ADOPT) core measures: Environmental do-
150. Müller MJ, Enderle J, Pourhassan M, et al. Metabolic adaptation to main. Obesity 26: S35–S44, 2018.
caloric restriction and subsequent refeeding: The Minnesota Starvation 176. Sainsbury A, Evans IR, Wood RE, et al. Effect of a 4-week weight
Experiment revisited. Am J Clin Nutr 102: 807–819, 2015. maintenance diet on circulating hormone levels: Implications for clinical
151. Müller MJ, Enderle J, Bosy-Westphal A. Changes in energy expenditure weight loss trials. Clin Obes 5: 79–85, 2015.
with weight gain and weight loss in humans. Curr Obes Rep 5: 413–423, 177. Sainsbury A, Wood RE, Seimon RV, et al. Rationale for novel in-
2016. termittent dieting strategies to attenuate adaptive responses to energy
152. Murphy CH, Hector AJ, Phillips SM. Considerations for protein restriction. Obes Rev 19(Suppl 1): 47–60, 2018.
intake in managing weight loss in athletes. Eur J Sport Sci 15: 21–28, 178. Samaha FF, Iqbal N, Seshadri P, et al. A low-carbohydrate as compared
2015. with a low-fat diet in severe obesity. N Engl J Med 348: 2074–2081, 2003.
153. Nackers LM, Ross KM, Perri MG. The association between rate of initial 179. Schübel R, Nattenmüller J, Sookthai D, et al. Effects of intermittent and
weight loss and long-term success in obesity treatment: Does slow and continuous calorie restriction on body weight and metabolism over 50
steady win the race? Int J Behav Med 17: 161–167, 2010. wk: A randomized controlled trial. Am J Clin Nutr 108: 933–945,
154. Norén E, Forssell H. Very low calorie diet without aspartame in obese 2018.
subjects: Improved metabolic control after 4 weeks treatment. Nutr J 13: 180. Schwartz MW, Seeley RJ, Zeltser LM, et al. Obesity pathogenesis: An
77, 2014. endocrine society scientific statement. Endocr Rev 38: 267–296, 2017.
155. O’Rourke RW. Metabolic thrift and the genetic basis of human obesity. 181. Schwarz NA, Rigby BR, La Bounty P, Shelmadine B, Bowden RG. A
Ann Surg 259: 642–648, 2014. review of weight control strategies and their effects on the regulation of
156. Paddon-Jones D, Westman E, Mattes RD, et al. Protein, weight man- hormonal balance. J Nutr Metab [Internet] 2011: 237932, 2011.
agement, and satiety. Am J Clin Nutr 87: 1558S–1561S, 2008. 182. Seimon RV, Wild-Taylor AL, Keating SE, et al. Effect of weight loss via
157. Pardue A, Trexler ET, Sprod LK. Case study: Unfavorable but severe vs moderate energy restriction on lean mass and body composition
transient physiological changes during contest preparation in a drug- among postmenopausal women with obesity: The TEMPO diet ran-
free male bodybuilder. Int J Sport Nutr Exerc Metab 27: 550–559, domized clinical trial. JAMA Netw Open 2: e1913733, 2019.
2017. 183. Shah M, Vella A. Effects of GLP-1 on appetite and weight. Rev Endocr
158. Peos JJ, Helms ER, Fournier PA, Sainsbury A. Continuous versus in- Metab Disord 15: 181–187, 2014.
termittent moderate energy restriction for increased fat mass loss and fat 184. Silva AM, Júdice PB, Carraça EV, King N, Teixeira PJ, Sardinha LB.
free mass retention in adult athletes: Protocol for a randomised con- What is the effect of diet and/or exercise interventions on behavioural
trolled trial—the ICECAP trial (Intermittent versus Continuous Energy compensation in non-exercise physical activity and related energy ex-
restriction Compared in an Athlete Population). BMJ Open Sport Exerc penditure of free-living adults? A systematic review. Br J Nutr 119:
Med 4: e000423, 2018. 1327–1345, 2018.
159. Peos J, Norton L, Helms E, Galpin A, Fournier P. Intermittent dieting: 185. Siw Eriksson L, Olsson M, Björkman O. Splanchnic metabolism of
Theoretical considerations for the athlete. Sports 7: 22, 2019. amino acids in healthy subjects: Effect of 60 hours of fasting. Metabolism
160. Peos J, Brown AW, Vorland CJ, Allison DB, Sainsbury A. Contrary to 37: 1159–1162, 1988.
the conclusions stated in the paper, only dry fat-free mass was dif- 186. Slavin JL. Position of the American Dietetic Association: Health impli-
ferent between groups upon reanalysis. Comment on: “Intermittent cations of dietary fiber. J Am Diet Assoc 108: 1716–1731, 2008.
energy restriction attenuates the loss of fat-free mass in resistance 187. Spiller RC, Trotman IF, Higgins BE, et al. The ileal brake—Inhibition of
trained individuals. A randomized trail”. J Funct Morphol Kinesiol 5: jejunal motility after ileal fat perfusion in man. Gut 25: 365–374, 1984.
85, 2020. 188. Strasser B, Spreitzer A, Haber P. Fat loss depends on energy deficit only,
161. Pfluger PT, Kampe J, Castaneda TR, et al. Effect of human body weight independently of the method for weight loss. Ann Nutr Metab 51:
changes on circulating levels of peptide YY and peptide YY3-36. J Clin 428–432, 2007.
Endocrinol Metab 92: 583–588, 2007. 189. Sumithran P, Prendergast LA, Delbridge E, et al. Long-term persistence of
162. Phillips SM, Chevalier S, Leidy HJ. Protein “requirements” beyond the hormonal adaptations to weight loss. N Engl J Med 365: 1597–1604, 2011.
RDA: Implications for optimizing health. Appl Physiol Nutr Metabol 41: 190. Sundfør TM, Svendsen M, Tonstad S. Effect of intermittent versus
565–572, 2016. continuous energy restriction on weight loss, maintenance and car-
163. Poddar M, Chetty Y, Chetty VT. How does obesity affect the endocrine diometabolic risk: A randomized 1-year trial. Nutr Metab Cardiovasc
system? A narrative review. Clin Obes 7: 136–144, 2017. Dis 28: 698–706, 2018.
164. Poortmans JR, Carpentier A, Pereira-Lancha LO, Lancha A. Protein 191. Sutin AR, Boutelle K, Czajkowski SM, et al. Accumulating data to op-
turnover, amino acid requirements and recommendations for athletes timally predict obesity treatment (ADOPT) core measures: Psychosocial
and active populations. Braz J Med Biol Res 45: 875–890, 2012. domain. Obesity 26: S45–S54, 2018.
2980
192. Thomas DT, Erdman KA, Burke LM. American College of Sports 201. Westerterp-Plantenga MS, Lejeune MPGM, et al. High protein intake
Medicine joint position statement. Nutrition and athletic performance. sustains weight maintenance after body weight loss in humans. Int J
Med Sci Sports Exerc 48: 543–568, 2016. Obes 28: 57–64, 2004.
193. Toomey CM, Cremona A, Hughes K, Norton C, Jakeman P. A review of 202. Weyer C, Walford RL, Harper IT, et al. Energy metabolism after 2 y of
body composition measurement in the assessment of health. Top Clin energy restriction: The Biosphere 2 experiment. Am J Clin Nutr 72:
Nutr 30: 16–32, 2015. 946–953, 2000.
194. Trexler ET, Smith-Ryan AE, Norton LE. Metabolic adaptation to 203. Wing RR, Jeffery RW. Prescribed “breaks” as a means to disrupt weight
weight loss: Implications for the athlete. J Int Soc Sports Nutr 11: 1–7, control efforts. Obes Res 11: 287–291, 2003.
2014. 204. Wolfe RR, Miller SL. The recommended dietary allowance of protein: A
195. Tumova E, Sun W, Jones PH, et al. The impact of rapid weight loss on misunderstood concept. JAMA 299: 2891–2893, 2008.
oxidative stress markers and the expression of the metabolic syndrome in 205. Woods SC, D’Alessio DA. Central control of body weight and appetite.
obese individuals. J Obes 2013: 729515, 2013. J Clin Endocrinol Metab 93: s37–s50, 2008.
196. van Baak MA. Meal-induced activation of the sympathetic nervous 206. Worku MG, Seretew WS, Angaw DA, Tesema GA. Prevalence and as-
system and its cardiovascular and thermogenic effects in man. Physiol sociated factor of Brown adipose tissue: Systematic review and meta-
Behav 94: 186, 2008. analysis. Biomed Res Int, 2020.
197. Veronese N, Solmi M, Caruso MG, et al. Dietary fiber and health out- 207. Wren AM, Seal LJ, Cohen MA, et al. Ghrelin enhances appetite and
comes: An umbrella review of systematic reviews and meta-analyses. Am increases food intake in humans. J Clin Endocrinol Metab 86: 5992,
J Clin Nutr 107: 436–444, 2018. 2001.
198. Verreijen AM, Engberink MF, Memelink RG, et al. Effect of a high 208. Wycherley TP, Moran LJ, Clifton PM, Noakes M, Brinkworth GD. Ef-
protein diet and/or resistance exercise on the preservation of fat free mass fects of energy-restricted high-protein, low-fat compared with standard-
during weight loss in overweight and obese older adults: A randomized protein, low-fat diets: A meta-analysis of randomized controlled trials.
controlled trial. Nutr J 16: 1–8, 2017. Am J Clin Nutr 96: 1281–1298, 2012.
199. von Loeffelholz Christian, and Andreas Birkenfeld. The Role of Non- 209. Yao M, Roberts SB. Dietary energy density and weight regulation. Nutr
Exercise Activity Thermogenesis in Human Obesity, Endotext. Kenneth Rev 59: 247–258, 2009.
R Feingold, et. al. ed: MDText.com, Inc., 2018. 210. Yumuk V, Tsigos C, Fried M, et al. European guidelines for obesity
200. Wang L, Rhodes CJ, Lawrence JC. Activation of mammalian target of management in adults. Obes Facts 8: 402–424, 2015.
rapamycin (mTOR) by insulin is associated with stimulation of 4EBP1 211. Zhang Y, Proenca R, Maffei M, et al. Positional cloning of the
binding to dimeric mTOR complex 1. J Biol Chem 281: 24293–24303, mouse obese gene and its human homologue. Nature 372: 425–432,
2006. 1994.
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Brief Review

Metabolic Adaptations to Weight Loss: A Brief

Other Hormones Involved in Physiological Adaptations to Nutritional Strategies to Reduce Metabolic

Figure 3. A theoretical framework of metabolic adaptation. Note how increases in

intake. These results add up to the idea that increased protein

foods in someone’s diet, also known as glycemic load (GL) (11),

Eur J Appl Physiol 97: 225–238, 2006.

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