Weight Loss Plateau: Reasons, Challenges, and Solutions: A Narrative Review

ABSTRACT

Background and Aim

Weight loss plateau (WLP) is one of the most significant obstacles for individuals with overweight and obesity during weight loss (WL). Preventing WLP is essential for maintaining long‐term WL and minimizing the risk of weight regain. Despite the widespread challenge of combating obesity and barriers to WL, this area has received limited attention in research. Therefore, the present narrative review discusses the reasons, challenges, and management of WLP, which often occurs alongside diet‐induced WL.

Methods

A comprehensive literature search was conducted using search strategies and keywords to identify studies published until January 2025 in several databases. Data were synthesized using a narrative review approach. Given the descriptive and exploratory nature of this review, no formal methodological quality or risk of bias assessment was performed for the included studies.

Results

WLP typically emerges approximately 6–8 months into WL programs, although this timeline may vary among individuals. In addition to individual differences related to WLP, even with adherence to dietary and lifestyle modifications, WLP can occur primarily due to metabolic adaptations. These adaptations occur because a reduction in dietary intake decreases all components of total energy expenditure (TEE). Furthermore, calorie restriction can increase appetite and hunger. Reductions in TEE, combined with increased appetite, contribute to the development of an energy gap. Factors such as initial WL, previous WL experiences, a tendency toward passive overconsumption of calories, behavioral changes and genetic factors can contribute to an earlier WLP. Although all components of TEE decrease during WL, the most significant reduction is often observed in non‐exercise activity thermogenesis (NEAT).

Conclusion

Several strategies may help address metabolic adaptation and prevent and manage WLP. These include caloric reduction, high‐protein diets, gradual WL, planned overfeeding, increased physical activity, maintenance of reduced body weight, body recomposition, nonlinear dieting approaches, and appetite‐regulating dietary plans.

Abbreviations

AMPK

AMP‐activated protein kinase

AT

Adaptive thermogenesis

BMR

Basal metabolic rate

CCK

Cholecystokinin

CICO

Calories in, calories out

CNS

Central nervous system

EAT

Exercise activity thermogenesis

EE

Energy expenditure

FFM

Fat‐free mass

FM

Fat mass

GI

Glycemic index

GLP‐1

Glucagon‐like peptide‐1

IER

Intermittent energy restriction

MPS

Muscle protein synthesis

mTORC1

Mechanistic target of rapamycin complex 1

NEAT

Non‐exercise activity thermogenesis

PA

Physical activity

PYY

Peptide YY

QoL

Quality of life

REE

Resting energy expenditure

TEE

Total energy expenditure

TEF

Thermic effect of food

WL

Weight loss

WLP

Weight loss plateau

1. Introduction

Obesity is a global public health concern and a risk factor for chronic conditions, including cardiovascular disease, type 2 diabetes, and certain cancers [1, 2]. Weight loss (WL) is a crucial strategy for improving clinical outcomes and enhancing the quality of life (QoL) of individuals with obesity [3, 4, 5]. However, maintaining WL over the long term is challenging [6]. Interventions for obesity often result in initial rapid WL, followed by a period of weight stabilization and subsequent gradual weight regain [6].

Many individuals with obesity struggle to achieve and sustain WL despite their efforts [7]. A meta‐analysis of 29 long‐term WL studies showed that more than half of the WL achieved was typically regained within 2 years, with over 80% regained by the fifth year [8]. Another meta‐analysis reported that individuals with overweight and obesity may return to their baseline weight within 1 year after a nutritional WL intervention [9]. An analysis of 155 studies found that participants in behavioural weight management programmes regained approximately 0.9 kg during the first year after programme completion [10]. In addition, around 85% of individuals on WL diets experience a WL plateau (WLP), a period during which WL slows or stops despite ongoing weight‐management efforts [11].

WLP refers to a period during a WL intervention in which reductions in body weight stall despite continued adherence to a caloric deficit and physical activity (PA) plan [12]. Understanding the factors contributing to WLP can help develop strategies to overcome these obstacles and achieve sustained WL in individuals with obesity. Several reviews have explored strategies to prevent WLP [6, 13, 14]; however, their findings are inconsistent. Therefore, this narrative review aimed to provide robust evidence and insights into the mechanisms underlying WLP, as well as the challenges and strategies for addressing WLP during weight management in individuals with overweight and obesity.

1.1. Clinical Importance of Preventing and Managing WLP

WLP significantly affects long‐term weight management, particularly in individuals with higher initial weights [11]. Its onset may mark a transition toward weight regain and undermine efforts to sustain WL. Therefore, preventing WLP is important for improving long‐term WL outcomes [6].

WL improves risk factors associated with chronic diseases, including dyslipidemia, hyperglycemia, inflammation, oxidative damage, and hypertension [15]. Even a modest 5%–10% reduction in body weight provides significant benefits, with greater WL potentially producing additional improvements [16, 17, 18, 19]. Further WL is accompanied by reductions in total energy expenditure (TEE), which contribute to the development of WLP [20]. Therefore, addressing WLP is crucial for maximizing the benefits of WL and reducing the risk of chronic diseases [21].

1.2. Timing and Onset Patterns of WLP During WL

The misconception that minor dietary changes produce continuous WL was based on Wishnofsky's 3,500‐calorie rule, which estimated that one pound of WL occurs per 3,500 kcal of energy deficit [22]. Based on this rule, simply reducing four servings of grains (approximately 320 kcal) from the daily diet could result in nearly 15 kg of WL in 1 year and 30 kg over 2 years [6]. However, contemporary understanding reveals that the simplistic calculations used in such WL guidelines are flawed because WL does not occur in a linear manner [23, 24].

Individuals undergoing moderate calorie restriction report experiencing WLP within 12 weeks [25]. However, a meta‐analysis of eight WL strategies, including diet alone, diet combined with exercise, exercise alone, meal replacements, very‐low‐energy diets, and weight‐loss medications (such as orlistat and sibutramine), showed that WL typically reaches a plateau around 6 months after intervention initiation, regardless of the intervention type [26]. Another study found a plateau after 8 months, with 12.4% WL achieved at that time [27]. Multiple WLPs may occur during long‐term WL, with each plateau lasting longer than the previous one [25].

Several individual characteristics may influence the timing of WLP onset. Naturally lean individuals [28, 29], women, and older adults [30, 31] tend to reach a plateau earlier due to metabolic and behavioral factors. Intermittent non‐adherence, low PA, reduced non‐exercise activity thermogenesis (NEAT), lower basal metabolic rate (BMR), lower muscle mass, and genetic factors may accelerate WLP onset [29, 32, 33, 34].

1.3. Determinants and Predictors of Variability Among Individuals in WLP

Multiple factors contribute to individual variability in the onset and magnitude of WLP, including early WL response, weight suppression and previous WL history, subtle increases in energy intake, psychological and behavioral factors, and genetic or epigenetic differences. These determinants interact in complex ways and can help explain why some individuals reach a plateau earlier or regain weight more rapidly. A summary of these predictors is illustrated in Figure 1, and detailed descriptions are provided in the Supplementary File.

Figure 1.

Predictors of individual differences in WLP.

1.4. Understanding False WLP

WLP occurs when body weight remains unchanged for 1 month or longer. Among resistance athletes, short‐term weight stability may result from body recomposition [35]. Furthermore, it is common for adults to experience daily weight fluctuations of up to 2 kg, often due to factors such as changes in bladder volume, the presence of food in the digestive system, and alterations in extracellular fluid resulting from carbohydrate intake [36]. To accurately monitor weight, it is recommended to weigh oneself daily in the morning, after using the bathroom, before consuming anything, and while unclothed, and to record each measurement [37]. In addition, the menstrual cycle affects water retention and subsequent weight fluctuations in women [38]. A study reported that among 69 females who recorded their daily body weight over 4 months, 20% experienced their highest weight just before menstruation, while 43.5% recorded their highest weight during the initial days of menstruation [39]. Another study noted daily weight fluctuations of 0.59–2.07 kg in women throughout the menstrual cycle, with weight typically increasing before menstruation [40].

1.5. Does WLP Extend Beyond the “Calories In, Calories Out” Theory?

The “calories in, calories out” (CICO) paradigm [41] underscores the significance of both calorie intake and energy expenditure (EE). Calorie intake primarily comprises energy derived from food and beverages. In contrast, EE encompasses several components, including resting EE (REE), the thermic effect of food (TEF), exercise activity thermogenesis (EAT), and NEAT [42, 43]. Caloric restriction is a crucial element in the prevention and management of obesity based on the concept that obesity arises from a sustained positive energy balance [44]. Consequently, this paradigm posits that dietary interventions for WL are effective only if they significantly reduce energy intake and/or enhance EE [45]. Therefore, WLP may occur when a new equilibrium point in energy balance is established (Figure 2).

Figure 2.

WL initially occurs due to a calorie deficit (energy out > intake); however, over time, reduced EE leads to a new balance, resulting in WLP.

There are two main perspectives regarding the relationship between calorie intake and EE. The first is the static (linear) energy balance model, which assumes that changes in calorie intake do not lead to adaptive changes in EE [29]. As discussed above, Wishnofsky's rule exemplifies this static assumption by predicting linear WL in response to a given energy deficit; however, observed WL is typically lower than predicted by the static model [46, 47, 48]. In contrast, the dynamic (non‐linear) energy balance model recognizes that biological and behavioral adaptations occur in response to changes in energy intake and expenditure [29]. Reductions in calorie intake trigger compensatory decreases in EE through mechanisms such as adaptive thermogenesis (AT) and reduced PA [46]. In reality, energy balance is dynamic, and caloric restriction influences all components of TEE. Figure 3 illustrates the differences between the dynamic and static models in the context of WL [29].

Figure 3.

Comparison of dynamic and static WL models. The dynamic model (blue) shows that the WL progressively slows and stabilizes over time, whereas the static model (red) assumes a continuous linear decline, overestimating long‐term WL.

The WLP concept appears to challenge the static or linear interpretation of CICO theory, which is commonly used in discussions of weight management and loss [46]. However, this simplistic approach overlooks individual variability and the numerous factors that influence energy intake and expenditure [49]. Importantly, the principle of CICO remains valid when considered within the dynamic energy balance framework. Within this framework, WLP occurs when energy intake during a negative energy balance reaches a level equivalent to the energy requirements for weight maintenance. This phenomenon occurs because reductions in caloric intake can influence EE in complex and sometimes unexpected ways.

1.6. The Reasons for WLP

EE components involved in WLP development. AT, a reduction in EE greater than expected based on body composition, plays a central role [50, 51]. Despite preserving fat‐free mass (FFM), EE decreases due to reductions in REE, NEAT, EAT, and TEF. These changes occur particularly in the early stages of caloric restriction, with REE decreasing by 100–500 kcal/day below predicted values [52, 53, 54]. NEAT is particularly variable and may decline by 30% or more after modest WL, contributing significantly to the TEE reduction [55]. Together, these adaptations result in lower‐than‐expected EE that slows further WL and promotes weight regain unless offset by high PA or continued energy restriction. This explains why WLP occurs even when individuals appear to have an energy deficit. A summary of these EE changes and their contributions to WLP is presented in Figure 4, and detailed descriptions and supporting references are provided in the Supplementary File.

Figure 4.

Summary of the primary mechanisms leading to reduced EE and the onset or persistence of WLP.

1.7. The Role of Appetite Regulation in the Development of WLP

WLP is often influenced by intermittent non‐adherence to prescribed dietary and PA regimens, which many individuals fail to recognize, as well as by misreporting of dietary intake and PA [56]. For example, individuals with obesity who reported a history of diet resistance underreported their energy intake by an average of 47% and overreported their PA by 51% [57]. Another study reported that WLP most commonly occurs between 1 and 2 years after WL initiation and is driven primarily by intermittent non‐adherence to the prescribed dietary (energy intake) plan rather than by metabolic adaptation [32].

Eating behavior is regulated by hormonal signals, hypothalamic circuits, and reward systems [58], all of which are disrupted during calorie restriction, leading to increased hunger and heightened food reward [59, 60, 61, 62]. WL alters circulating nutrients and affects brain centers controlling energy balance [63, 64], while also shifting hormones such as ghrelin, leptin, insulin, glucagon‐like peptide‐1 (GLP‐1), cholecystokinin (CCK), and peptide YY (PYY) [59, 65, 66, 67, 68, 69]. These changes promote increased food intake and eating frequency [70, 71, 72], contributing to WLP [51, 73]. For each kilogram of WL, appetite may increase by approximately 100 kcal/day, whereas EE decreases by only 20–30 kcal/day, highlighting the greater influence of appetite on weight regulation [74].

Unlike lean individuals, those with obesity may not show reduced hunger after overeating, thereby increasing the risk of WLP [75, 76]. The “energy gap” emerges from reduced EE and increased appetite during energy restriction (Figure 5) [69], thereby impairing adherence, especially in obesogenic environments [77, 78]. The body's regulatory mechanisms that defend body weight create this gap [79], a phenomenon further explained by the dual‐intervention theory, which balances the risks of starvation and predation while environmental and behavioral factors determine weight within this range [80, 81].

Figure 5.

During WL, reduced EE (due primarily to lower NEAT and REE) and increased hunger create an “energy gap” that promotes WLP and potential weight regain.

2. Solutions for WLP

Several evidence‐based strategies have been proposed to prevent and manage WLP. These strategies should address the decline in EE, increased appetite, metabolic adaptation, and energy gaps that occur during the WL period. Evidence from clinical populations with overweight or obesity suggests that the strategies discussed below may help prevent and manage WLP.

2.1. Caloric Reduction and the Re‐Establishment of a Caloric Deficit

Further caloric restriction is a common strategy for managing WLP. However, WLP may persist despite low caloric intake, often reducing adherence [13]. However, severe caloric restriction can worsen metabolic adaptations and widen the energy gap, complicating WL and increasing the risk of WLP [82]. To reduce diet fatigue, individuals often switch between WL diets (e.g., low‐fat vs. low‐carb); however, without further caloric reduction, such changes do not resolve WLP [83]. A recent trial indicated that WLP occurring at approximately 6 months is largely influenced by physiological factors and cannot be overcome merely by alternating diets without further caloric reductions [84]. Transitioning from one healthy diet to another without further reducing caloric intake did not lead to sustained or accelerated WL after 6 months [84]. While reducing calorie intake is a key strategy for addressing WLP, excessively low intake can increase the risk of nutrient deficiency, trigger stronger metabolic adaptations, and reduce adherence in the long term.

2.2. High‐Protein Diets

A high‐protein diet is defined as one that exceeds 1.2 g/kg/day and comprises 20% of total energy intake [85]. Such diets may attenuate the loss of FFM, which constitutes 20%–30% of body mass and declines during caloric restriction [86, 87, 88, 89, 90, 91]. This preservation may involve the modulation of muscle protein synthesis (MPS), AMP‐activated protein kinase (AMPK), and mechanistic target of rapamycin complex 1 (mTORC1) [92, 93]. Because FFM loss accounts for approximately one‐third of REE reduction following WL [94, 95], high‐protein diets can help maintain REE, with reports indicating an average increase of ~142 kcal/day compared with standard protein diets [96]. They also increase TEE through increased TEF, which ranges from 0% to 3% for fats, 5%–10% for carbohydrates, and 20%–30% for proteins [97]. For instance, theoretically, doubling protein intake from 400 to 800 kcal/day can increase TEF by ~80 kcal [28]. Although this may represent a small fraction of TEE, its impact may be significant over an extended period. Additionally, proteins provide greater satiety per calorie than carbohydrates or fats, thereby helping to reduce energy intake [98, 99, 100]. In individuals with overweight or obesity, higher protein intake enhances satiety and fullness [101], possibly via improved leptin sensitivity in the central nervous system (CNS) [102].

2.3. Gradual WL

Calorie restriction lowers REE, with greater deficits leading to larger reductions in REE [103, 104]. Gradual WL approaches may better preserve FFM than rapid WL [105, 106], as rapid WL has been linked to a greater decline in REE and 0.74 kg more FFM loss, according to a meta‐analysis [107]. As FFM plays a key role in metabolic rate, its loss contributes to a reduction in REE [108]. Moreover, animal studies suggest that hunger may persist after rapid WL [70, 109]. Therefore, gradual WL may help reduce the energy gap by preserving FFM, maintaining REE, and limiting post‐WL hunger.

2.4. Overfeeding

Intentional overfeeding, commonly used by athletes such as bodybuilders, has been shown to promote lean mass gains, but it is also associated with fat gain [110, 111, 112]. Reverse dieting, a controlled caloric increase, has been proposed to increase FFM with only a modest increase in FM [113, 114]. However, individual responses vary, with weight gains ranging from 1.8 to 8.1 kg following 6–12 weeks of overfeeding [110, 111, 115, 116, 117]. Higher protein intake during overfeeding may reduce variability in weight gain and favor FFM accretion over fat accumulation [111, 118, 119]. Typically, lean mass accounts for only 30%–40% of total weight gain during overfeeding, depending on the dietary regimen [120]. Protein overfeeding appears to be more effective than carbohydrate or fat overfeeding in increasing FFM and may not increase FM [112].

Overfeeding for more than 4 weeks has been reported to increase REE by 5%–12% [111, 115, 116, 121, 122, 123, 124, 125], whereas low‐protein overfeeding diets did not increase REE compared with the 160 and 227 kcal/day increases observed with normal‐ and high‐protein overfeeding diets [111]. REE increases have been reported after weight gain in both normal‐weight and obese individuals, although larger gains may produce only modest additional increases in REE [123, 126]. Responses may also vary by age and weight status, with differences reported between adolescents and adults and between normal‐weight and obese populations [127, 128].

Animal studies have shown appetite suppression after overfeeding; however, human data are inconsistent [129]. For example, reduced energy intake was observed after 21 days of overeating [130], whereas no change was identified after 13 days of 35% overfeeding [131]. This difference may reflect stronger appetite compensation in obesity‐resistant individuals than in those predisposed to obesity [132].

2.5. Increase Levels of Physical Activity

PA is the second major contributor to TEE after REE [133], with EAT accounting for 15%–30% of TEE in regularly active individuals [134, 135]. Resistance training may help preserve REE by maintaining FFM, which is a key determinant of REE [136, 137]. However, increased PA does not always lead to higher TEE due to compensatory adjustments in EE [138], potentially regulated by the activity state theory, which suggests a theoretical control center that regulates EE by adjusting PA levels to maintain a specific set point [139]. Over time, sustained exercise may induce physiological adaptations, including reduced sympathetic activity during standardized exercise tasks [54] thereby improving exercise efficiency [140].

NEAT varies from 6% to 10% of TEE in sedentary people to over 50% in very active individuals [137, 141]. Simple lifestyle changes, such as using stairs or taking walking breaks, can boost NEAT [142], and it has been hypothesized that this may enhance WL maintenance more effectively than strict dietary restriction alone [143, 144]. Resources are available to quantify NEAT and guide strategies to mitigate metabolic adaptation [145, 146].

In general, increasing non‐exercise PA by 30%–50% or more has been recommended to address the post‐WL energy gap. However, even a ~100% rise in activity failed to reverse metabolic adaptation after ~60 kg of WL, as shown in the “The Biggest Loser” study [147].

2.6. Maintaining Reduced Body Weight

During weight maintenance, TEE remains suppressed due to reduced NEAT, increased muscle efficiency, and lower leptin and thyroid hormone levels, leading to decreased sympathetic activity [23, 95, 148]. Reductions in REE and non‐REE components may persist for more than 1 year in individuals who maintain a reduced body weight [23, 50]. This metabolic adaptation can continue long‐term and may remain more pronounced than expected based on pre‐WL levels [46]. It has been suggested that only weight regain, rather than weight maintenance, can reduce metabolic adaptation [149]. However, the primary advantage of maintaining weight in the WLP is to prevent weight regain, rather than to mitigate metabolic adaptation or increase REE, NEAT, or TEE (Figure 6).

Figure 6.

During early WL, metabolic adaptation lowers REE, while body weight and FFM decrease rapidly and FM decreases gradually. During subsequent WL, these variables continue to decline until reaching WLP, after which they become relatively stable during weight maintenance.

2.7. Body Recomposition

Body recomposition, which involves simultaneous fat loss and muscle gain, has gained attention as a potential strategy for WLP [35, 150]. Slight calorie increases (~100 kcal/day) may not always lead to weight gain because of potential compensatory increases in EE [151]. When combined with a high‐protein diet and resistance training, this approach may support recomposition by increasing FFM and associated EE.

Theoretically, body recomposition may help reduce the energy gap by increasing FFM and the EE associated with FFM, as well as by influencing appetite through increased energy intake. Intakes above 2.0 g/kg/day of protein and higher resistance training volume have been suggested as key factors [152]. This strategy may be more feasible in certain populations, such as beginners and athletes increasing training load; however, evidence supporting its application in individuals with overweight or obesity is limited [35]. Tracking lean mass via regular bioelectrical impedance may be useful for monitoring progress [153].

2.8. Non‐Linear Diet Strategies

Non‐linear dietary strategies, also known as diet periodization or intermittent energy restriction (IER), such as diet breaks and refeeds [154, 155], involve alternating between periods of energy restriction and higher energy intake, differing from continuous energy restriction while maintaining a comparable overall energy deficit [36].

Dietary refeeding, a common IER strategy, involves increasing total energy and carbohydrate intake by approximately 5%–10% for 1–3 days during a period of caloric deficit [156, 157]. This approach may help preserve FFM [158], enhance WL by attenuating muscle protein breakdown through elevated insulin levels [159, 160], while partially restoring anabolic signaling [161, 162]. Carbohydrate intake may increase leptin levels [163] more than fat [164], potentially benefiting individuals with overweight or obesity, especially those with leptin resistance [165]. FM reductions lower circulating leptin concentrations, thereby contributing to AT. Leptin administration during weight maintenance partially reverses the decline in EE and improves skeletal muscle efficiency [166, 167], highlighting its role in mediating WL‐induced metabolic adaptation [167]. Multi‐day refeeds may help preserve FFM and metabolic rate [168, 169, 170, 171], although the findings are inconsistent [164, 172].

A diet break is a dietary strategy that involves a consecutive period of four or more days, potentially extending to several weeks, during which individuals consume weight‐maintenance calories or slightly above. This approach requires adherence to specific calorie and macronutrient targets per day as part of a WL plan [156]. However, a recent meta‐analysis found no significant improvement in body composition following diet breaks or continuous energy restriction [173]. Nevertheless, diet breaks may provide psychological advantages that support adherence and help mitigate adaptive reductions in REE [174], thereby reducing the energy gap.

2.9. Appetite‐Reduced Dietary Strategies

Dietary WL not only increases hunger and food cravings [73, 175] but also enhances the preference for high‐calorie foods, particularly sweet snacks [176]. Fiber‐rich diets, characterized by vegetables, fruits, whole grains, and legumes, are recommended [177]. Higher dietary fiber intake has been associated with modest WL (~0.35 kg over 6–8 weeks) [178, 179] and a reduction in overall energy intake [180, 181, 182, 183].

Low‐glycemic‐index (GI) diets have been hypothesized to increase satiety and reduce hunger through their effects on gastrointestinal function and blood glucose regulation [184, 185, 186]. A meta‐analysis reported that low‐GI diets are associated with modest but statistically significant WL in interventions lasting at least 4 weeks [184].

Low‐energy‐density diets, rich in filling foods like salads, soups, and low‐fat dairy, help reduce hunger and subsequent energy intake [99, 187, 188, 189, 190]. Compared with high‐density snacks, low‐density high‐protein options such as yogurt increase satiety [191]. In addition, drinking water before meals has been shown to lower meal energy intake and support WL [192, 193, 194].

3. Strengths and Limitations

This review synthesizes diverse studies to provide a broad perspective on the challenges and potential strategies related to WL and WLP. This study highlights areas requiring further research and explores behavioral strategies to prevent WLP. However, the study selection and interpretation may be subject to bias. As a narrative review, this study did not perform formal methodological quality or risk of bias assessments; therefore, the findings should be interpreted cautiously and complemented by more rigorous research.

4. Conclusion

WLP is a predictable stage of WL that commonly occurs within the first year of intervention, typically after 6–8 months, when further changes in body weight and composition are limited. Its onset is influenced by factors including early WL response, weight suppression history and previous WL attempts, a tendency toward passive overconsumption of calories, psychological and behavioral factors, and genetic and epigenetic variability. Within the CICO framework, WLP reflects the establishment of a new energy balance, with reductions in NEAT representing the predominant component, followed by changes in REE and, to a lesser extent, EAT and TEF. Appetite‐related adaptations also play a central role, as increased hunger and reduced TEE create an “energy gap” that challenges adherence and increases the risk of weight regain after WL. Effective management requires addressing both physiological and behavioral adaptations rather than simply increasing caloric restriction. Established strategies include restoring energy deficits, optimizing protein intake, using gradual WL approaches, increasing resistance training or daily activity, and maintaining reduced body weight. Emerging approaches, including controlled overfeeding, body recomposition, non‐linear dietary strategies, and appetite‐reduced dietary strategies, may offer additional benefits but require further investigation. A multifaceted, physiology‐informed approach is essential for improving long‐term adherence and sustainably maintaining weight.

Author Contributions

Damoon Ashtary‐Larky: conceptualization, methodology, investigation, writing – original draft, writing – review and editing. Shooka Mohammadi: writing – review and editing, investigation, supervision.

Funding

The authors have nothing to report.

Ethics Statement

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Transparency Statement

Shooka Mohammadi affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; no important aspects of the study have been omitted; and any discrepancies from the study as planned have been explained.

Supporting information

Supporting File

Data Availability Statement

Data sharing does not apply to this article, as no datasets were generated or analyzed during the current study.