Obesity Reviews最新文献

Introduction: Community- and population-level and policy interventions are commonly evaluated using nonrandomized studies (NRS), rather than randomized trials (RCTs). Recent Cochrane reviews of interventions for preventing childhood obesity have been restricted to RCTs, so less is known about the effectiveness of these more upstream interventions. To address this gap, we conducted an overview of reviews of NRS interventions (NRSI), which assessed change in BMI in children and adolescents aged 5-18 years and compared NRSI findings with those from RCTs.

Methods: We searched five databases up to November 2024. Screening, data extraction, and quality assessment were performed using standardized tools.

Results: We included 28 systematic reviews and identified 136 NRSI either based in school (n = 118), community (n = 4) or combined settings (n = 14) and evaluating policy (n = 48), education (n = 11), or a combined intervention (n = 77). Twenty-six reviews included both NRSIs and RCTs; of these, 12 reported meta-analyses. Findings were largely unchanged when we excluded the RCTs and re-ran analyses. Overall, study-level results from the NRSI favored the intervention group; a quarter favored the comparison group. The meta-analysis summary effects from NRSIs were consistent with two recently published Cochrane meta-analyses of RCTs of obesity prevention interventions.

Conclusions: The results from this overview of reviews suggest researchers and policy makers can be confident in considering the results of robust nonrandomized study designs (evaluating their impact on BMI) alongside RCTs in their decision making. Although we identified a significant number of NRSIs for review, very few evaluations of upstream interventions were eligible for inclusion.

Introduction: While the association between metabolic factors and risk of colorectal cancer (CRC) in the general population is well established, their effect on precancerous polyps among individuals undergoing surveillance colonoscopy is not well understood. Additionally, most guidelines do not consider metabolic factors when determining surveillance colonoscopy intervals. This systematic review and meta-analysis summarizes current evidence for this association in individuals at above-average risk for CRC.

Methods: Relevant studies published from 2010 through 2023 were identified using seven databases. Two independent reviewers performed abstract and full-text screening and quality assessment. Effect estimates were reported using a pooled odds ratio (POR) or pooled hazard ratio (PHR) based on the primary studies measurement with 95% confidence intervals and heterogeneity was reported as I².

Results: 15,486 studies were screened, with 24 meeting the inclusion criteria. General obesity (POR = 1.31, 95% CI 1.09-1.57, I² = 67%), central obesity (POR = 1.31, 95% CI 1.16-1.49, I² = 0%), hypertension (POR = 1.22, 95% CI 1.02-1.44, I² = 57%), high triglyceride (POR = 1.39, 95% CI 1.06-1.83, I² = 0%), and metabolic syndrome (PHR = 1.24, 95% CI 1.01-1.51, I² = 24%) were significant risk factors for the development of any precancerous polyp. The association between diabetes and nonalcoholic fatty liver disease and overall precancerous polyps was inconsistent. General obesity (PHR = 3.04, 95% CI 2.01-4.60, I² = 0%) but not diabetes (PHR = 1.07, 95% CI 0.72-1.57, I² = 0%) was significantly associated with the risk of advanced precancerous polyps.

Conclusion: Metabolic factors should be considered when recommending surveillance colonoscopy intervals, which in most guidelines are mainly determined based on the findings at colonoscopy, the significance of family history of CRC and genetic predispositions.

Obesity is a major risk factor for metabolic disorders and cancer, largely due to dysregulated nutrient sensing and metabolic reprogramming. Acyl-CoA synthetase short-chain family member 2 (ACSS2) is a key enzyme that converts acetate into acetyl-CoA, fueling de novo lipogenesis and histone acetylation. In obesity, ACSS2 expression is transcriptionally induced by sterol regulatory element-binding proteins (SREBPs) and carbohydrate response element-binding protein (ChREBP), while phosphorylation and dephosphorylation at specific residues (e.g., S659, S263, and T363) further modulate its enzymatic activity and subcellular localization. Emerging evidence shows the pathogenic roles of ACSS2 in obesity-related disorders through its dual regulation of lipid synthesis and epigenetic modification. In most obesity-associated cancers, ACSS2 is upregulated in tumor cells to enhance acetate utilization and promote growth. By contrast, in digestive system tumors, ACSS2 downregulation enables metabolic plasticity by shifting from acetate metabolism toward aerobic glycolysis, thereby favoring malignant progression. Concurrently, ACSS2 downregulation in T cells under chronic antigen exposure compromises antitumor immunity, underscoring its context-dependent role in shaping tumor metabolism and immune evasion. Notably, its nuclear localization is frequently associated with greater malignancy and poorer prognosis. Stratified analyses further suggest its prognostic value may be enhanced in individuals with obesity. Although ACSS2 inhibitors have shown therapeutic promise in preclinical studies, only one has progressed to clinical trials, highlighting the need for continued translational research. This review summarizes current insights for obesity-evoked metabolic disorders and cancer progression linked by ACSS2 and suggests future studies on understanding ACSS2 regulatory mechanisms, therapeutic potential, and biomarker utility across obesity-associated diseases.

Obesity as a chronic and multifactorial disease requires a multidisciplinary team acting together in a holistic multitarget intervention. Multidisciplinary therapy targeting obesity and its complications includes physical exercise, nutritional, and behavior counseling. When lifestyle changes are not sufficient in adults, medication prescription and bariatric surgery may be recommended. The aim of this narrative review is to summarize the underlying mechanisms and effects of multidisciplinary therapy in the control of obesity and its complications in adults. [Correction added on 21 January 2026, after first online publication: The previous sentence has been corrected in this version.] All types of clinical studies developed in an adult population were included. Different types of multidisciplinary therapy (short- and long-term) in the primary and secondary settings were identified. Multidisciplinary therapy seems to be useful in the control of adverse effects of obesity, including reductions in biomarkers of inflammation, cardiometabolic risk factors, dyslipidemia, diabetes, hypertension, metabolic syndrome, nonalcoholic fatty liver diseases, atherosclerosis, cardiovascular disease, obstructive sleep apnea, and psychosocial outcomes. These results highlight the importance of targeting obesity and its complications in a holistic approach with a multidisciplinary team acting together.

The strength of the association between achieving clinically significant weight loss and remission of metabolic complications remains unclear. This rapid review aimed to investigate the effect of weight loss on remission of metabolic risk factors. We searched Embase, Medline, Web of Science, and Google Scholar databases (up to June 2025) for studies comparing the effects of ≥ 5% versus < 5% total weight loss (%TWL) for at least 12 months. Mean differences (MD) and risk ratios (RR) with 95% confidence intervals (95% CI) were calculated for the meta-analysis. A total of 43 comparative studies were reviewed. Compared to < 5%TWL, ≥ 5%TWL had a higher RR of type 2 diabetes remission (RR = 7.88: 95% CI = 5.00, 12.43; I² = 75.2%), hypertension remission (RR = 2.23: 95% CI = 1.06,4.68; I² = 70.5%), and metabolic syndrome remission (RR = 5.61: 95% CI = 1.62,19.49; I² = 70.2%). Compared to < 5%TWL, ≥ 5%TWL participants achieved significant MDs in HbA1c (MD = -1.06: 95% CI = -1.40, -0.71), fasting plasma glucose (MD = -1.13: 95% CI = -1.84, -0.43), systolic blood pressure (MD = -3.65: 95% CI = -5.56, -1.74), diastolic blood pressure (MD = -3.26: 95% CI = -6.31, -0.20), triglycerides (MD = -0.26: 95% CI = -0.45, -0.06), and HDL-cholesterol (MD = 0.09: 95% CI = 0.04, 0.14). Remission of metabolic complications and improvements in HbA1c, blood pressure, lipids, and fasting insulin were observed following ≥ 5%TWL in people with obesity in a dose-response manner. Factors like the %TWL achieved (particularly ≥ 15%), bariatric surgery, and duration of follow-up predict these outcomes.

Background: The relationship between obesity and traumatic brain injury is complex and not fully understood. While obesity is commonly linked to worse outcomes, conflicting data support the "obesity paradox," with higher body mass index showing protective effects.

Methods: We identified patients with traumatic brain injury and defined two propensity score-matched cohorts: patients with normal weight and patients with obesity. Outcomes were compared using risk estimates, odds ratios, Kaplan-Meier survival analysis, and log-rank testing.

Results: Obesity was associated with slightly lower risks of the following: • Pneumonia (5.1% vs. 3.4%, OR 1.53 [95% CI: 1.015-2.297], p = 0.041), • Acute kidney injury (9.3% vs. 6.8%, OR 1.41 [95% CI: 1.047-1.908], p = 0.023), • Myocardial infarction (3.4% vs. 1.7%, OR 2.04 [95% CI: 1.182-3.503], p = 0.009), • Cognitive deficits (16.9% vs. 11.9%, OR 1.52 [95% CI: 1.201-1.914], p < 0.001), • Cardiac arrest (2.5% vs. 0.8%, OR 3.05 [95% CI: 1.485-6.272], p = 0.001), • Emergency department visits or admissions (16.1% vs. 12.7%, OR 1.32 [95% CI: 1.046-1.661], p = 0.019), • Emergency procedures (16.1% vs. 11.9%, OR 1.43 [95% CI: 1.127-1.803], p = 0.003), • Twist drill/burr hole procedures (1.7% vs. 0.8%, HR 2.67 [95% CI: 1.045-6.827], p = 0.033 by log-rank test), • Mortality was not significantly different.

Conclusions: Patients with obesity exhibited a lower incidence of selected complications, supporting the obesity paradox in neurotrauma. However, that did not translate into differences in mortality or functional outcomes. Body mass index may not fully capture the complexities of body composition or functional reserve, highlighting the need for studies using comprehensive adiposity and metabolic measures. Given multiple outcomes tested and modest effect sizes, these findings should be interpreted cautiously.

Objective: Depression and obesity represent major public health challenges, and their comorbidity suggests underlying shared mechanisms. A comprehensive understanding of the common cognitive-behavioral and neurobiological pathways, particularly those involving reward processing, is essential for developing effective clinical and public health interventions. This systematic review synthesizes evidence regarding the overlap of behavioral and neural substrates or correlates of reward processing and manifestations in depression and obesity.

Results: The findings indicate that comorbid depression and obesity are associated with reward-related behaviors, as well as functional and structural alterations in key reward-processing regions, such as the hippocampus, amygdala, and anterior cingulate cortex. These alterations correlate with increased severity of depressive symptoms and abnormal reward-related behaviors. Insulin resistance and dysregulation of serotonin pathways constitute significant mediators that exacerbate reward dysfunction in affected individuals. Additionally, early-life stress and genetic predispositions significantly shape both the structure and function of the brain's reward circuitry.

Conclusions: This review highlights that the comorbidity of obesity and depression can be explained through complex behavioral and neural mechanisms, particularly those involving reward processing pathways. Further longitudinal and intervention studies are warranted to clarify causal relationships and underlying mechanisms.

Introduction: Metabolic syndrome (MetS) may be associated with obesity-related cancer (ORC) owing to shared risk factors like physical inactivity, insulin resistance, gut microbiome dysfunction, and inflammation. We conducted an umbrella review of systematic reviews with meta-analysis to synthesize the evidence on the association between MetS and ORC risk and survival.

Methods: Searches in five databases (Medline, Embase, CINAHL, Cochrane Library, and Scopus) retrieved 2524 systematic reviews with meta-analyses (SRMAs), which underwent title and abstract screening (2524), full-text review (41), and data extraction for included SRMAs (21). Summary effects and 95% confidence intervals were re-estimated using random-effects models. Methodological quality, certainty of evidence, and publication bias were assessed using the AMSTAR 2, modified Ioannidis criteria, and Egger's test, respectively.

Results: A total of 25 associations between MetS and ORC risk and five between MetS and survival were evaluated. Overall, 10 associations evaluating MetS and ORC risk were highly suggestive (four) or suggestive (six), while the rest were classified as weak (seven) or nonsignificant (eight). One association was suggestive for MetS and ORC survival, while the rest were classified as weak (three) or nonsignificant (one). The Egger's and excess significance tests were significant for 8(32%) associations between MetS and ORC risk and 3(60%) associations between MetS and ORC survival.

Conclusion: This umbrella review suggests metabolic syndrome increases the risk of several obesity-related cancers and worsens colorectal cancer survival. Despite study variability, consistent associations across diverse populations highlight the urgency of prevention and management strategies targeting metabolic dysfunction to reduce cancer burden. Summary In this umbrella review, highly suggestive and suggestive evidence supports associations between MetS and the risk and survival of several obesity-related cancers. However, a better understanding of the relationship between metabolic syndrome and obesity-related cancers is still needed to provide appropriate clinical care, design optimal interventions, and prevent subsequent increases in the risks of cancer, morbidity, and mortality.

Next-generation incretin therapies, including semaglutide and tirzepatide, have transformed obesity and Type 2 diabetes management. However, evidence-based nutritional strategies to support safe and effective use of these agents remain limited. To address this gap, we conducted a systematic scoping review across five databases of studies published between January 2015 and April 2025 to map and appraise clinical trials incorporating nutritional interventions or dietary assessments during semaglutide or tirzepatide therapy in adults with obesity or Type 2 diabetes. Eligible studies included adults receiving semaglutide or tirzepatide with either an active dietary intervention or measured nutrition-related outcomes. Study quality was assessed using established tools. Twelve studies were included: 10 randomized controlled trials, one non-randomized comparative study, and one cross-sectional observational study. Interventions ranged from structured very-low-energy or ketogenic diets to general lifestyle counseling and observational dietary assessments. Across studies, energy intake decreased by 24% to 39%, but lean tissue loss accounted for up to 40% of total weight reduction. Only three studies involved nutrition professionals, and systematic assessment of protein or micronutrient intake was rare. One observational study found widespread nutrient inadequacies and limited access to dietetic support. Despite the effectiveness of semaglutide and tirzepatide for weight loss, evidence on optimal dietary strategies is sparse. Early dietitian involvement, high-protein, nutrient-dense diets, and routine nutritional monitoring should be prioritized. Robust trials are needed to define best practice for integrating dietary care alongside pharmacotherapy.

Childhood and adolescent obesity poses health risks. Standardizing outcome measurements in physical activity interventions enhances evidence comparability. This study summarizes health outcomes reported in systematic reviews and classifies them under an existing taxonomy as a preliminary step toward the future development of a core outcome set. Eligible studies were systematic reviews with or without meta-analyses involving children and adolescents (4-19 years) with overweight or obesity, reporting health outcomes from physical activity interventions. Data extraction was performed independently in pairs, collecting study characteristics, intervention details, participant demographics, and outcomes. Outcomes were classified into taxonomy-based domains. This review identified key outcomes in body composition, lipid profile, blood pressure, and physical functioning. The most frequent body composition outcomes were BMI, body weight, and body fat. Lipid profile outcomes included HDL, total cholesterol, and LDL. Blood pressure outcomes comprised systolic and diastolic measurements. Physical functioning was assessed by time spent in physical activity. Among 137 reviews, 841 outcomes were extracted, identifying 169 unique outcomes across 16 domains. The most reported unique outcomes were BMI (52.6%), body weight, body fat, HDL, and systolic blood pressure. This study highlights the need for a Core Outcome Set to standardize outcomes in physical activity interventions for children with overweight or obesity.