Abstract
Early postoperative weight loss (EWL) after bariatric surgery is a critical as a powerful predictor of long-term weight loss and metabolic outcomes. This narrative review shows evidence from recent studies examining the biological, behavioral, and clinical implications of EWL in patients undergoing various bariatric procedures. We discuss the hormonal and metabolic adaptations that occur in the first months after surgery, the psychosocial and behavioral factors influencing postoperative outcomes, and how early weight loss can guide individualized management. We further conduct the clinical pathways that integrate EWL monitoring into routine postoperative care. The goal is to encourage standardization in EWL measurement and its integration into multidisciplinary bariatric management to improve patient postoperative outcomes.
Keywords: Bariatric surgery, Weight loss, Postoperative period, Predictive value of tests, Treatment outcome
INTRODUCTION
Obesity remains a significant global health problem, increasing the prevalence of type 2 diabetes mellitus, cardiovascular disease, obstructive sleep apnea, and certain cancers [1]. Bariatric surgery has proven to be the most effective long-term intervention for individuals with severe obesity, leading to substantial and sustained weight loss and improvement or remission of obesity-related comorbidities [2]. However, outcomes vary among patients, with some achieving optimal long-term results and others experiencing early weight plateau or significant weight regain [3]. The variability in outcomes has been conducted to identify early predictors of long-term success. One such promising predictor is early postoperative weight loss (EWL), measured in the first 1–6 months after surgery [4]. Early changes in body weight may reflect not only physiological responses to surgery but also the patient’s compliance to lifestyle recommendations [4,5]. Understanding the clinical significance of EWL can help healthcare providers apply timely interventions for patients at risk of unfavorable outcomes. Such interventions may range from nutritional counseling and behavioral modification to the early initiation of pharmacologic management or consideration of endoscopic procedures. By integrating EWL into routine follow-up protocols, clinicians can improve the personalization of postoperative care [6,7]. This review aims to provide a comprehensive information of EWL as a prognostic marker, exploring biological mechanisms, psychosocial determinants, and clinical applications [8,9].
PATTERNS AND PREDICTIVE VALUE OF EARLY WEIGHT LOSS IN BARIATRIC SURGERY
1. Measurements for early weight loss
Various measurements are used to quantify EWL, including percent total weight loss (%TWL), percent excess weight loss (%EWL), and changes in body mass index (BMI) [10,11]. While %EWL has historically been the most widely used measure, %TWL is preferred due to its simplicity, ease of comparison across different baseline BMIs, and reduced statistical bias. Despite the increasing use of %TWL, there remains a lack of consensus on optimal value for defining adequate early weight loss [12,13].
2. Patterns of early weight loss
Early weight loss refers to the amount of weight reduction achieved within the initial postoperative period, typically defined as the first 1–6 months following surgery. This period is characterized by rapid physiological and behavioral adjustments followed by a gradual deceleration in the rate of weight loss [14]. This pattern reflects a combination of surgical, physiological, and behavioral factors, including postoperative diet, hormonal adaptations, and patient compliance to lifestyle modifications [15]. Several studies indicate that the weight loss in this early window strongly predicts long-term success, with greater early reductions correlating with sustained outcomes at 1, 3, and even 5 years after surgery [1,6,7,8,16,17,18,19] (Table 1). Retrospective data from multi-center have shown that patients achieving at least 20–25% EWL at 3 months are significantly more likely to reach and maintain the value of ≥50% EWL at 1 year [20]. Furthermore, those who fall within the lowest quartile of early weight loss frequently demonstrate suboptimal long-term results, emphasizing the importance of early intervention for this group [21].
Table 1. Summary of key studies on early postoperative weight loss and long-term outcomes after bariatric surgery.
| First author (Year) | Study design | Sample size | Procedures | Definition of 'early' WL | Main outcome | Key findings |
|---|---|---|---|---|---|---|
| Tettero et al. (2022) [6] | Prospective cohort | 635 | RYGB, SG | %TWL at 3 months | %TWL at 1, 2, 5 years | Early %TWL strongly correlated with long-term %TWL; 3 months %TWL ≥20% predicted ≥25%TWL at 5 years |
| Manning et al. (2015) [7] | Retrospective cohort | 111 | RYGB, SG | %EWL at 6 weeks | %EWL within 2 years | Greater early %EWL predicted higher maximal %EWL |
| King et al. (2020) [8] | Prospective | 2,400 | RYGB, LAGB, SG | %WL at 3 months | %WL at 3–7 years | Strong dose–response relationship between early and long-term WL; effect strongest in RYGB |
| Mor et al. (2012) [16] | Retrospective | 201 | RYGB | %EWL at 6 weeks | %EWL at 1, 2, 5 years | Early %EWL ≥20% predicted sustained weight loss; slower early loss linked to higher long-term attrition |
| Sczepaniak et al. (2012) [17] | Retrospective | 310 | RYGB | %WL at 6 weeks | %WL at 1 year | Early %WL was an independent predictor of 1 year %WL |
| van de Laar et al. (2019) [18] | Multicenter retrospective | 5,967 | RYGB, SG | %WL at 6 weeks | %WL up to 7 years | Early %WL enabled categorization into 'fast' vs 'slow' responders; fast responders maintained better outcomes |
| Sugerman et al. (2003) [19] | Prospective cohort | 500 | RYGB | %EWL at 1 month | %EWL at 1, 5 years | 1 month %EWL significantly predicted long-term %EWL; lower early %EWL linked to limited sustained weight loss and metabolic improvements |
WL = weight loss, RYGB = Roux-en-Y gastric bypass, SG = sleeve gastrectomy, %TWL = percent total weight loss, %EWL = percent excess weight loss, LAGB = laparoscopic adjustable gastric banding.
Improvements in comorbidities such as type 2 diabetes, dyslipidemia, and hypertension often correlate with initial weight loss. Rapid early improvements in fasting glucose and hemoglobin A1c within the first postoperative month have been strongly linked to sustained type 2 diabetes remission [22]. Similarly, early reductions in triglycerides, low-density lipoprotein cholesterol, and systolic blood pressure predict durable cardiovascular benefits over several years [1]. From a methodological perspective, the use of standardized early weight loss thresholds allows for consistent prognostic assessments across different institutions and patient populations [23]. Advances in predictive analytics have allowed integration of early weight loss data with demographic, behavioral, and metabolic variables to predict long-term outcomes with high accuracy [22].
Interpretation of early weight loss should be approached with caution. Individual variability, influenced by factors such as baseline BMI, age, sex, and type of surgical procedure, can affect the rate of early weight loss [24,25]. Additionally, psychosocial and behavioral factors, including adherence to dietary guidelines and engagement in physical activity, can modulate outcomes [26].
3. Sleeve gastrectomy (SG) vs. Roux-en-Y gastric bypass (RYGB)
Randomized and prospective trials show rapid metabolic improvements after both SG and RYGB, with early restoration of postprandial glycemic control (lower glucose excursions and earlier insulin secretion), exaggerated glucagon-like peptide-1 (GLP-1)/peptide YY (PYY) peaks, and measurable reductions in energy intake appearing within the first postoperative weeks and consolidating across the subsequent 1–3 months as dietary progression advances [24,27,28,29,30]. These physiologic changes co-occur with faster gastric emptying (SG) and accelerated distal nutrient delivery (RYGB) that activate the ileal brake, alongside transient suppression of orexigenic tone, jointly shifting energy balance toward loss [24,28,29,30]. Pooled comparative evidence indicates that RYGB achieves a greater percentage of EWL and TWL than SG at 6–12 months. Beyond effect sizes are heterogeneous across studies and analysis, and the between-procedure gap frequently narrows over time as cohorts converge—reflecting baseline BMI mix and case severity, technical variation (bougie size, limb lengths), perioperative diet/behavioral protocols, and follow-up intensity [1,21,22].
At the “first-quarter” window (1–3 months), typical trajectories across mixed-BMI cohorts show ~13–15% EWL by 1 month and ~30–35% EWL by 3 months, but the spread is wide and systematically patterned: higher baseline BMI tends to inflate %EWL variability via the denominator effect; programmatic factors (perioperative diet progression, frequency/structure of follow-up), and patient-level behaviors (energy intake, protein adequacy, physical activity, self-monitoring) modulate early velocity, as do physiologic drivers such as early satiety and dumping-like responses [7,27,31,32]. By 6 months, many RYGB cohorts approach ~50–60% EWL and SG cohorts ~45–55% EWL; when expressed as %TWL these values are lower and less BMI-dependent, and absolute numbers vary with the EWL formula (e.g., ideal-weight anchor), the chosen reporting metric (%EWL vs. %TWL), and case-mix across centers [1,27,32,33]. Importantly, several Asian prospective cohorts observed near-equivalent 1–3-month EWL between SG and RYGB despite procedural differences, implying that early outcomes are explained more by metabolic responsiveness, adherence behaviors, and intensity of clinical contact than by procedure choice alone during this window [32].
4. One-anastomosis gastric bypass (OAGB) and biliopancreatic diversion with duodenal switch (BPD-DS)
OAGB integrates restrictive gastric pouching with a comparatively longer biliopancreatic limb than standard RYGB, yielding a stronger malabsorptive component and more pronounced enteroendocrine/bile acid signals (e.g., GLP-1, PYY, fibroblast growth factor 19 [FGF19]) in the early postoperative months [34,35]. In randomized and multicenter series, OAGB was non-inferior to RYGB for early outcomes and in several analyses numerically favored at 6–12 months. Quantitatively, OAGB at 6–12 months shows comparable or greater %EWL than RYGB (pooled means approximately 50–55% %EWL in mixed-BMI cohorts) [34,35]. BPD-DS and single anastomosis duodeno–ileal bypass with sleeve gastrectomy (SADI-S) variants deliver some of the steepest early and durable weight losses through potent malabsorption and marked bile-acid signaling shifts; however, they carry increased risks of protein-calorie malnutrition, deficiencies of fat-soluble vitamins (A, D, E, K) and trace elements (iron, zinc, selenium), diarrhea/steatorrhea, and bone disease, making lifelong, protocolized monitoring and aggressive supplementation obligatory. BPD-DS (including SADI-S) achieves some of the steepest early losses, with 6-month %EWL typically in the mid-40s to 50s depending on baseline BMI class [36,37,38].
5. Prognostic value of early weight loss
Recent meta-analyses evaluating postoperative weight loss patterns have demonstrated a biphasic curve: a rapid early loss phase during the first 6–12 months, driven largely by caloric restriction and hormonal shifts, followed by a plateau phase and, in some cases, gradual regain thereafter. A 2021 network meta-analysis of more than 20,000 patients reported that at 6 months, mean %EWL ranged from 48–52% for SG and 55–62% for RYGB, with the gap between procedures narrowing at 12–24 months [3]. Importantly, the early slope of %EWL, particularly in the first 3–6 months, was strongly associated with long-term weight maintenance, underscoring its value as a prognostic marker. Another comprehensive systematic review of randomized and non-randomized trials concluded that %TWL measured at 3 months is a reliable predictor of 2–5-year outcomes across different bariatric procedures [39].
Several large cohort studies have validated EWL as a robust long-term prognostic marker. In a multicenter study of 1,200 RYGB patients, those achieving ≥25% EWL at 3 months had a 5-year success rate (>50% EWL maintained) exceeding 80%, whereas fewer than 40% of patients below this threshold sustained long-term success [31]. Beyond a single cutoff, grouping patients into quartiles or deciles showed a clear stepwise pattern. Every additional 5–10% of EWL at 3 months predicted better 5-year outcomes in both %EWL and %TWL [7]. Similarly, a prospective SG cohort showed that 3-month %EWL predicted not only 2-year weight outcomes but also remission or improvement of type 2 diabetes, hypertension, and dyslipidemia after multivariable adjustment for age, sex, baseline BMI, medication use, and procedure-related factors [27]. Importantly, the prognostic signal of early EWL persisted after accounting for behavioral adherence metrics (dietary protein intake, self-monitoring frequency, physical activity), operative details (bougie size, limb lengths), and center-level effects, supporting a biologically grounded mechanism rather than a mere proxy for follow-up intensity [33]. A pooled analysis of >15,000 patients further confirmed that early high responders (top quartile of %EWL at 3 or 6 months) consistently achieved superior long-term weight and metabolic outcomes across subgroups (sex, age strata, baseline BMI classes, procedure type), in internal and external validations and acceptable calibration across deciles of predicted risk [32].
BIOLOGICAL MECHANISMS OF EWL
The early postoperative phase following bariatric surgery is characterized by rapid and profound physiological changes that extend beyond simple caloric restriction [40]. The biological basis of EWL is multifactorial, involving anatomical restriction, hormonal adaptations, and changes in bile acid metabolism and the gut microbiome.
1. Gut hormone
One of the most notable mechanisms is the alteration of gut hormone profiles, increases in GLP-1 and PYY, which reduce appetite [28]. SG and RYGB markedly increase postprandial GLP-1 and PYY concentrations within the first postoperative month, with rises detectable as early as one week in some studies [24,28,29]. In RYGB, rapid nutrient delivery to the distal small intestine activates the “ileal brake,” provoking exaggerated L-cell secretion and larger postprandial excursions of GLP-1 and PYY; this augments early-phase insulin secretion, improves β-cell function and hepatic insulin sensitivity, and reinforces satiety [28,29]. This lead to enhanced satiety and improved glycemic control. SG produces qualitatively similar incretin elevations, most likely via accelerated gastric emptying and altered small-bowel transit that increase distal nutrient exposure; concurrent suppression of gastric fundus-derived ghrelin further potentiates satiety signaling [24,29,41,42]. Physiologic studies indicate that the amplitude of the GLP-1/PYY response is generally greater after RYGB than SG, particularly during the first 1–3 postoperative months, aligning with steeper early reductions in energy intake and better early glycemic control [28,29,30]. Additionally, both procedures can enhance glucose-dependent insulinotropic polypeptide (GIP) responses, although the metabolic impact of GIP appears less consistent than that of GLP-1 in this context [24,28].
Ghrelin, a potent orexigenic hormone primarily secreted by X/A-like cells in the gastric fundus, is sharply reduced after SG due to resection of this anatomical region, resulting in a pronounced and sustained attenuation of hunger signals, improved portion control, and greater ease in meeting prescribed dietary goals [24,42]. The suppression of circulating ghrelin levels is often detectable within days postoperatively and may persist for years, contributing to the early satiety profile typical of SG patients. In RYGB, ghrelin levels also fall in the immediate postoperative period, likely due to altered gastric anatomy, reduced functional fundus volume, and changes in vagal afferent signaling, but they tend to return toward baseline within several months to years as compensatory secretion from residual gastric tissue and other sites occurs [43]. Both surgical patterns of ghrelin modulation interact with concurrent rises in anorexigenic hormones such as GLP-1 and PYY, synergistically reducing caloric intake, improving appetite regulation, and facilitating strict adherence to dietary restrictions during the critical early recovery and rapid weight loss phases.
2. Metabolic adaptation
Metabolic adaptations also play a crucial role in early weight loss [18]. Resting energy consumption often remains relatively preserved despite significant caloric deficits, partially due to improved mitochondrial function and increased fatty acid oxidation [11]. Changes in nutrient absorption also contribute, particularly after procedures with a malabsorptive component, such as Roux-en-Y gastric bypass [25]. Although the degree of malabsorption is modest in the early phase, it still provides an additive effect to caloric restriction, accelerating weight loss. Importantly, the rate and pattern of EWL vary by surgical technique, with bypass procedures often producing more rapid initial results compared to restrictive operations [12]. Neuroendocrine changes extend to the central nervous system, where functional imaging studies have documented altered activity in brain regions associated with reward and food cue processing [18]. These changes help diminish the impulse to eat, reinforcing the physiological satiety signals [11].
3. Bile acid signaling
Additionally, Bile acid signaling is altered after both RYGB and SG, with increased circulating bile acids activating receptors such as FXR and TGR5. RYGB markedly elevates circulating bile acids-particularly conjugated species such as taurocholic and glycocholic acids-and FGF19 concentrations within weeks of surgery, initiating potent metabolic signaling cascades through activation of the nuclear receptor FXR and the membrane receptor TGR5. These pathways modulate key processes including hepatic gluconeogenesis suppression, enhanced glycogen storage, improved lipid oxidation, and upregulated mitochondrial energy expenditure [30,44,45]. The activation of TGR5 on enteroendocrine cells also promotes GLP-1 secretion, which synergistically reinforces glycemic control and appetite suppression. In SG, postoperative bile acid changes have also been documented, though the direction, magnitude, and specific bile acid species affected vary considerably between studies, and overall shifts tend to be smaller than those observed after RYGB [44]. Moreover, emerging evidence suggests that bile acid–microbiota interactions, such as altered Firmicutes to Bacteroidetes ratios, may influence L-cell proliferation and incretin hormone release, further contributing to early weight loss and metabolic improvements. These insights highlight bile acid signaling as a potential therapeutic target for adjunctive pharmacologic strategies aimed at enhancing bariatric surgery outcomes [46].
4. Brain–gut axis and neural adaptation
Neuroimaging studies using functional magnetic resonance imaging and positron emission tomography have demonstrated altered activation patterns in key brain regions, such as the hypothalamus, striatum, and prefrontal cortex, which are associated with food reward valuation and cue reactivity after bariatric surgery [28,29]. These central changes appear within weeks and are closely linked to peripheral hormonal shifts. In particular, increased GLP-1 and PYY levels, along with modulation of dopaminergic pathways in the mesolimbic system, diminish the hedonic drive to consume calorie-dense foods and strengthen reinforcement of healthier eating behaviors [24,44]. Clinically, this manifests as earlier onset of satiety and in some cases conditioned aversive responses to high-sugar or high-fat foods, which can promote sustained adherence to postoperative dietary recommendations and support long-term weight control. Procedure-specific patterns have been noted: RYGB tends to show greater early attenuation of striatal reward responses to high energy food and a higher prevalence of conditioned aversion (dumping like symptoms), consistent with its exaggerated incretin and bile acid signaling, whereas SG shows more uniform reductions in hunger and cue reactivity that parallel sustained ghrelin suppression and rising GLP-1/PYY, with similar directionality but typically smaller effect sizes during months 1–3; over time, neural response profiles partially converge as behavioral routines consolidate [24,28,29,44].
5. Surgery specific mechanistic differences
RYGB combines potent incretin stimulation, substantial bile acid–mediated metabolic effects, and a measurable degree of macronutrient malabsorption, all of which work synergistically to produce a steeper and more sustained early weight loss compared to other bariatric procedures [39,47]. Mechanistically, the exaggerated postprandial GLP-1 and PYY response in RYGB not only suppresses appetite but also enhances insulin secretion and improves hepatic and peripheral insulin sensitivity, while the bile acid–FGF19–FXR/TGR5 signaling axis further augments energy expenditure and lipid oxidation. The modest malabsorptive component reduces calorie and fat absorption, contributing additively to negative energy balance. In SG, the predominant drivers are marked ghrelin suppression due to surgical removal of the gastric fundus and robust, sustained increases in satiety-related hormones (GLP-1, PYY) that reduce caloric intake, improve meal pattern control, and reinforce dietary adherence [24,29,42]. Although bile acid changes occur in SG, their magnitude is typically less than after RYGB, and there is minimal malabsorption. OAGB and BPD-DS amplify bile acid circulation shifts through longer biliopancreatic limb lengths and induce a stronger malabsorptive effect, which accelerates early weight loss and can result in higher remission rates of obesity-related comorbidities. However, this comes at the cost of a substantially elevated risk of protein-calorie malnutrition, fat-soluble vitamin deficiencies (A, D, E, K), and trace mineral depletion (iron, zinc, selenium), necessitating vigilant, lifelong nutritional surveillance, individualized supplementation, and structured multidisciplinary follow-up [33,35,36,37].
Finally, inflammatory markers, including C-reactive protein and interleukin-6, typically decrease within weeks after surgery, reflecting a rapid attenuation of obesity-related systemic inflammation [48]. This reduction in inflammation not only improves overall metabolic health but may also facilitate better postoperative recovery [12]. Understanding these mechanisms is critical, as they form the biological basis for early weight loss and may inform the plan to optimize surgical outcomes and enhance postoperative management [9,49,50,51].
PSYCHOSOCIAL AND BEHAVIORAL FACTORS FOR EARLY POSTOPERATIVE COURSE
EWL is not only a physiological phenomenon; it is shaped by psychosocial and behavioral factors [26]. Patients’ motivation, health education, and preoperative expectations play important roles in shaping postoperative compliance to dietary and physical activity recommendations [15]. Some studies suggests that individuals with realistic expectations and strong intrinsic motivation are more likely to achieve greater early weight loss [11]. Preoperative counseling that includes behavior change strategies and individualized goal-setting has been shown to strengthen these factors, leading to improved short-term outcome and long-term maintenance [26].
Mental health status, particularly the presence of anxiety, depression, or binge-eating disorder, has a significant impact on EWL [15]. Unaddressed psychological comorbidities can lead to suboptimal compliance and hinder weight reduction [26]. Integrating psychological screening and therapy into perioperative care has been shown to enhance early weight loss and improve overall quality of life [18]. For example, cognitive-behavioral therapy targeting maladaptive eating patterns has been associated with improved early dietary adherence and reduced binge episodes after surgery [15]. Behavioral adaptability during the early postoperative phase is crucial [26]. Patients who can earlier modify eating patterns and incorporate physical activity into daily routines tend to achieve greater early weight loss. Structured behavioral interventions, including cognitive-behavioral therapy and motivational interviewing, can accelerate this adaptability [11,15]. Furthermore, personalized coaching with structured follow-up programs and multidisciplinary teams supports during the first 3 months can help patients overcome individual barriers and establish sustainable habits [52].
CLINICAL IMPLICATIONS OF MONITORING FOR EARLY WEIGHT LOSS
Integrating EWL monitoring into postoperative care pathways allows for proactive management of at-risk patients. For those identified as early slow responders, strategies may include intensified nutritional counseling, structured behavioral interventions, and pharmacologic therapies such as GLP-1 receptor agonists [20,53]. Conversely, high responders may be counseled on strategies to maintain momentum without compromising nutritional status [11]. This risk-stratified approach aligns with personalized medicine principles, ensuring resources are allocated effectively according to patient need [6]. Multidisciplinary teams can tailor interventions to address the specific needs of each patient, whether related to dietary habits, psychological barriers, or anatomical factors. In some cases, endoscopic or surgical revisions may be necessary to address anatomical issues contributing to poor EWL [54,55]. The frequency of follow-up visits should be adjusted based on EWL trajectories, with more frequent monitoring for patients who are not meeting expected milestones [56,57].
CURRENT LIMITATION AND FUTURE DIRECTIONS
Despite the growing recognition of EWL as a prognostic tool, significant research gaps remain. The lack of standardized definitions and measurement protocols limits the comparability of findings across studies [58]. Future research should aim to establish consensus on optimal EWL metrics and thresholds, validated across diverse patient populations and surgical techniques. Randomized controlled trials are needed to assess whether early interventions in slow responders improve long-term outcomes [27,59]. Longitudinal studies incorporating multi-omics profiling, neuroimaging, and psychosocial assessments could provide deeper insights into mechanisms that sustain weight loss beyond the early phase [26]. Further investigation into the biological mechanisms linking EWL to sustained metabolic benefits is warranted. This includes exploring the roles of gut hormones, bile acid signaling, microbiome alterations, and neural pathways [60].
Advances in artificial intelligence and machine learning are enabling the development of individualized prognostic tools that combine early weight loss data with demographic, behavioral, and metabolic variables to forecast long-term success [50]. These tools may eventually allow clinicians to adjust follow-up frequency, dietary prescriptions, and physical activity recommendations in real time, based on patient-specific risk profiles [15].
CONCLUSION
EWL loss serves as both a short-term success marker and a guide for long-term patient management after bariatric surgery. In clinical practice, monitoring EWL provides an opportunity for risk stratification and timely intervention. Patients demonstrating slower-than-expected progress can be targeted for more intensive dietary counseling, behavioral therapy, or pharmacologic support. This strategic approach highlights the clinical utility of early weight loss as both a marker of success and a tool for personalized postoperative management.
Footnotes
Funding: No funding was obtained for this study.
Conflict of Interest: The author has no conflict of interest.
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