INTRODUCTION
Obesity contributes to carcinogenesis through interconnected metabolic, inflammatory, immune, and hormonal pathways. 1 - 3 Based on this rationale, epidemiologic studies link adiposity to higher cancer incidence across multiple sites. 4 , 5 In this narrative review, we synthesize recent meta-analyses and selected cohort studies, focusing on the 13 cancers designated by the U.S. National Cancer Institute (NCI) as obesity-associated. 6 We also review emerging associations for additional cancers and appraise evidence on whether intentional weight loss, pharmacotherapy, and bariatric surgery can reduce cancer risk.
MECHANISMS LINKING OBESITY AND CANCER
The mechanisms linking obesity and cancer are complex and include disturbances in systemic metabolism, chronic inflammation, impairment of anti-tumor immunity, and hormonal imbalances ( Fig. 1 ). 1 - 3 , 7 , 8
Systemic metabolic disturbance
Obesity induces metabolic disturbances characterized by insulin resistance, elevated insulin-like growth factor-1 (IGF-1) levels, hyperinsulinemia, and altered lipid metabolism, which create a local tumor-promoting microenvironment. 1 - 3 , 7 Metabolic dysregulation can activate phosphatidylinositol-3 kinase/Akt/mammalian target of rapamycin pathway, thereby reinforcing cancer-associated metabolic reprogramming at the systemic level. 1 , 9 Furthermore, hypoxia induced by excess body fat accumulation facilitates angiogenesis, invasion, and survival of tumor cells by stimulating the expression of hypoxia-inducible factors ( Fig. 1 ). 2 , 3
Chronic inflammation
Low-grade inflammation resulting from excess adiposity promotes adipose tissue remodeling toward a pro-inflammatory phenotype. 1 , 2 , 8 Dysregulation of adipokine secretion further contributes to chronic inflammation and carcinogenesis. 1 - 3 , 7 Pro-tumorigenic adipokines, such as leptin, interleukin-1 beta (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α), can activate the nuclear factor kappa-light-chain-enhancer of activated B cells pathway and cyclooxygenase-2 production, both of which play pivotal roles in obesity-induced chronic inflammation. 1 - 3 , 7 In contrast, the level of adiponectin—an anti-tumorigenic adipokine—is decreased in obesity. 1 , 2 , 7 The infiltration of M1-polarized macrophages, differentiation of T helper 1 (Th1) and Th17 cells, and the release of pro-inflammatory cytokines, including interferon-gamma, IL-1β, IL-2, IL-6, IL-17, and TNF-α, further exacerbate chronic inflammation ( Fig. 1 ). 1 , 7 , 10
Impairment of anti-tumor immunity
Obesity-associated impairment of anti-tumor immunity also facilitates carcinogenesis. This includes inactivation of natural killer cells and the exhaustion and lipid deprivation of cytotoxic CD8 + T-cells. Furthermore, an increased number of myeloid-derived suppressor cells suppresses anti-tumor immune responses, thereby promoting tumorigenesis ( Fig. 1 ). 1 , 11
Hormonal imbalances
Hormonal imbalances in obesity are implicated in cancer development. 1 , 2 Elevated IGF-1 levels and hyperinsulinemia are associated with glucose metabolism dysregulation and contribute to a pro-inflammatory state. 1 , 2 In addition, increased estrogen levels in obese patients, particularly after menopause, are linked to the development of hormone-sensitive cancers. 2 , 12 Excess estrogens bind to estrogen receptors in breast, endometrial, and ovarian tissues, thereby activating cell proliferation, which can ultimately result in carcinogenesis. 2 , 12 Alterations in gastrointestinal hormones—such as ghrelin and cholecystokinin (CCK)—can also impair anti-inflammatory activity by inhibiting M2 macrophage polarization and Th2 cell differentiation. 2 Notably, elevated CCK levels in pancreatic tissue have been associated with pancreatic hyperplasia and carcinogenesis ( Fig. 1 ). 13
EPIDEMIOLOGICAL EVIDENCE FOR A LINK BETWEEN OBESITY AND CANCER RISK
In this narrative review, we summarize and evaluate recent epidemiological evidence linking obesity, measured specifically by body mass index (BMI) and waist circumference (WC), and cancer. We review recent meta-analyses, as well as notable cohort studies published from 2015 onwards, especially focusing on Asian data. This review is narrative and is not intended to be a systematic review.
As of 2025, 13 cancers have been established as obesity-associated by the NCI: (1) esophageal adenocarcinoma, (2) gastric cardia cancer, (3) colorectal cancer (CRC), (4) hepatocellular carcinoma, (5) pancreatic cancer, (6) gallbladder cancer, (7) postmenopausal breast cancer, (8) ovarian cancer, (9) endometrial cancer, (10) renal cell carcinoma, (11) thyroid cancer, (12) meningioma, and (13) multiple myeloma. Additionally, emerging epidemiological evidence has indicated potential associations between obesity and several other cancer types. 6
Esophageal cancer
Associations between esophageal cancer and obesity can differ by histologic subtype, but the association between obesity and esophageal adenocarcinoma is well established.
Two recent meta-analyses have evaluated the relationship between BMI and esophageal cancer, but neither clearly distinguished between adenocarcinoma and squamous cell carcinoma (SCC). One meta-analysis published in 2024 was based on only two studies that used a BMI ≥30 kg/m 2 cutoff; it reported a significantly increased overall risk (relative risk [RR], 1.65; 95% confidence interval [CI], 1.36 to 1.99). 4 In contrast, a meta-analysis published in 2025 included five studies and found no significant association (RR, 1.05 in males; RR, 0.99 in females). 5 The discrepancy between these findings could be due to the lack of histologic stratification, and the small number of studies in the former analysis raises concerns about a potential overestimation of risk.
A pooled analysis of Japanese cohorts, which included a larger number of studies and reflects a population in which SCC is prevalent, did not observe a meaningful association between BMI and esophageal cancer risk. 14 This likely reflects the predominance of SCC in East Asian populations, where the relationship with obesity is weaker than or even inverse to that in Western populations. Notably, however, a Korean cohort study using WC as the exposure metric found a significant increase in esophageal cancer risk (RR, 1.29; 95% CI, 1.23 to 1.36), even though SCC accounts for approximately 89.9% of cases in that population. 15 These findings suggest that alternative adiposity measures, such as central obesity indicators, might better capture the obesity-cancer link than BMI, particularly in SCC-dominant populations. The overall study characteristics are shown in Table 1 . 2 , 5 , 14 - 17
Gastric cancer
Gastric cancer differs in its pathogenesis depending on tumor location (cardia vs. non-cardia) and Helicobacter pylori infection status, and its association with obesity also varies accordingly.
Meta-analyses evaluating general obesity (as measured by BMI) have reported inconsistent results regarding gastric cancer risk. A 2024 meta-analysis involving four studies reported an RR of 1.43 (95% CI, 1.20 to 1.70) for individuals with BMI ≥30 kg/m 2 , 4 indicating a significant association, whereas a subsequent 2025 meta-analysis involving 10 studies found no statistically significant association, though it showed a similar trend. 5
Given these inconsistencies and the potential influence of tumor location, we examined subgroup analyses from cohort studies. A Japanese cohort study found that the risk was somewhat higher for the cardia region (RR, 1.53; 95% CI, 0.84 to 2.80 for males; RR, 1.73; 95% CI, 0.70 to 4.27 for females) and also tended to be slightly elevated for the non-cardia region (RR, 1.22; 95% CI, 0.96 to 1.57 for males; RR, 1.07; 95% CI, 0.73 to 1.58 for females), but the wide CIs precluded confirmation of statistical significance. 18 The overall study characteristics are shown in Table 1 . 4 , 5 , 16 - 20
Colorectal cancer
Meta-analyses of general obesity (BMI) consistently indicate an increased risk of CRC. A 2025 meta-analysis of 26 studies reported a pooled RR of 1.37 (95% CI, 1.24 to 1.50) for BMI ≥30 kg/m 2 versus <25 kg/m 2 , 3 and another 2025 meta-analysis of 66 studies found a similar or stronger association (RR, 1.57; 95% CI, 1.38 to 1.78). 21 Regarding body fat distribution, a large Korean cohort using BMI-adjusted WC showed higher risks in a highest versus lowest quintile comparison (RR, 1.40; 95% CI, 1.34 to 1.50 for males; RR, 1.19; 95% CI, 1.13 to 1.26 for females)—supporting the contribution of central adiposity beyond that of overall adiposity. 17 The overall study characteristics are shown in Table 1 . 2 , 5 , 16 , 17 , 21 - 27
Liver cancer
Meta-analytic evidence supports a positive association between liver cancer and general obesity. In a 2025 meta-analysis of 10 studies, males with BMI ≥30 kg/m 2 had a pooled RR of 1.72 (95% CI, 1.48 to 2.00) versus males with BMI <25 kg/m 2 , comparable to females, who showed an RR of 1.82 (95% CI, 1.72 to 1.92). 5
Results from a large UK Biobank study also suggest a stronger association in males than in females. For BMI (Q4 vs. Q1, sex-specific quartiles), the RR was 1.72 (95% CI, 1.10 to 2.66) in males and 0.87 (95% CI, 0.49 to 1.53) in females. For central adiposity measured by WC (Q4 vs. Q1), the RR was 1.64 (95% CI, 1.05 to 2.58) in males and 1.03 (95% CI, 0.58 to 1.81) in females. 28 These sex-divergent estimates in a Western cohort raise the possibility that the obesity-liver cancer relationship varies by sex and geographic region. In females, although not statistically significant, the slightly higher point estimate with WC than with BMI likely reflects that WC better captures visceral adiposity—which may be more directly linked to hepatic carcinogenesis through insulin resistance and inflammation—whereas BMI reflects overall mass. As females typically have greater subcutaneous fat distribution than males, WC may more sensitively detect metabolically adverse central adiposity than BMI.
Targeted, sex-stratified analyses in diverse populations are warranted to clarify this pattern. The overall study characteristics are shown in Table 2 . 5 , 16 , 17 , 28 - 31
Gallbladder cancer
A global pooled analysis of 27 cohorts showed that the risk of gallbladder cancer increased per 5 kg/m 2 increase in BMI for both sexes (RR, 1.27; 95% CI, 1.19 to 1.36), and central adiposity, assessed by WC, was likewise associated with an increased risk per 5 cm increase (RR, 1.15; 95% CI, 1.11 to 1.20). 32 An Asia-based pooled analysis of 14 cohorts reported an increased risk in females (RR, 1.41; 95% CI, 1.18 to 1.69) but not in males (RR, 1.01; 95% CI, 0.78 to 1.31) 33 ; however, that sex difference was inconsistent with the results of most previous studies. 17 , 34 Overall, the evidence indicates a positive association between gallbladder cancer risk and both general obesity and central adiposity. The overall study characteristics are shown in Table 2 . 17 , 31 - 35
Pancreatic cancer
Meta-analytic evidence on the association between obesity and pancreatic cancer is mixed. A 2025 meta-analysis including 10 studies reported a positive association with obesity (BMI ≥30 kg/m 2 vs. <25 kg/m 2 ), with an RR of 1.31 (95% CI, 1.15 to 1.48) in females and 1.26 (95% CI, 1.00 to 1.58) in males, 5 but a 2024 meta-analysis of three studies found no statistically significant association (RR, 1.10; 95% CI, 0.90 to 1.34) ( Table 2 ). 4
Notably, a large Swedish cohort study found no clear association when BMI was modeled categorically (BMI ≥30 kg/m 2 vs. <25 kg/m 2 ; RR, 1.36; 95% CI, 0.90 to 2.05) but a positive association in males when it was modeled continuously (per 5 kg/m 2 : RR, 1.40; 95% CI, 1.18 to 1.66). 20 Central adiposity (WC) remained associated after BMI adjustment in a Korean cohort (Q5 vs. Q1: RR, 1.21; 95% CI, 1.12 to 1.31 in males; RR, 1.16; 95% CI, 1.05 to 1.27 in females). 17
Overall, these findings suggest a tendency toward increased pancreatic cancer risk with higher BMI and central adiposity, although estimates of the scale of the increased risk vary across populations and modeling choices. Studies with rigorous confounder adjustment and diverse adiposity measures are needed. The overall study characteristics are shown in Table 2 . 4 , 5 , 16 , 17 , 20 , 36
Breast cancer
A 2024 meta-analysis of six studies on postmenopausal breast cancer reported a positive association for BMI ≥30 kg/m 2 versus <25 kg/m 2 (RR, 1.12; 95% CI, 1.07 to 1.18), 4 and an East Asian pooled analysis of 13 cohorts showed a stronger association (RR, 1.72; 95% CI, 1.43 to 2.06), with a similar pattern per 5 kg/m 2 increase (RR, 1.32; 95% CI, 1.25 to 1.39). 37 In contrast, a global pooled analysis of 16 premenopausal cohorts found an inverse association per 5 kg/m 2 BMI increase (RR, 0.87; 95% CI, 0.85 to 0.89). 38 Overall, the evidence indicates that BMI-related breast cancer risk differs by menopausal status—higher after menopause and lower before menopause. Mechanistically, after menopause, adipose tissue–mediated aromatization may increase estrogen production, and obesity-related insulin resistance and low-grade inflammation could foster a tumor-promoting milieu. 39 By contrast, before menopause, ovarian estrogen production exceeds any adipose tissue contribution; obesity-induced anovulation and lower bioavailable estradiol may therefore account for the inverse association. 40 The overall study characteristics are shown in Table 3 . 2 , 16 , 17 , 25 , 36 - 38 , 41 - 46
Endometrial cancer
A 2024 meta-analysis of two studies reported a markedly increased risk for BMI ≥30 kg/m 2 versus <25 kg/m 2 (RR, 3.80; 95% CI, 3.14 to 4.61). 4 Cohort data align with that finding: a United States study showed a higher risk per 1-standard deviation increase in baseline BMI (RR, 1.75; 95% CI, 1.49 to 2.06), 36 and a Korean cohort displayed elevated risks for BMI ≥25 kg/m 2 versus <23 kg/m 2 (RR, 1.63; 95% CI, 1.38 to 1.94) and central adiposity (WC) highest versus lowest quartile (RR, 1.90; 95% CI, 1.55 to 2.34). 47 Overall, both high BMI and central adiposity show a robust, dose-related association with endometrial cancer risk. The overall study characteristics are shown in Table 3 . 4 , 16 , 25 , 36 , 47 , 48
Ovarian cancer
Meta-analytic findings suggest that ovarian cancer has a small positive association with BMI, with the estimate of risk depending on how BMI is modeled. A 2016 global meta-analysis of 19 studies reported an RR of 1.05 (95% CI, 1.01 to 1.09) per 5 kg/m 2 increase. 49 In contrast, a 2024 meta-analysis of five studies using a categorical contrast (BMI ≥25 kg/m 2 vs. <23 kg/m 2 ) showed no statistically significant association (RR, 1.14; 95% CI, 0.95 to 1.37). 4 However, recent Korean cohort studies showed a higher risk with categorical BMI ≥25 kg/m 2 versus <23 kg/m 2 (RR, 1.19; 95% CI, 1.03 to 1.37) and BMI ≥30 kg/m 2 versus <25 kg/m 2 (RR, 1.42; 95% CI, 1.27 to 1.58) 50 and also a higher risk with abdominal obesity (WC ≥95 cm vs. 80–84.9 cm; RR, 1.23; 95% CI, 1.10 to 1.39). 50 Overall, in meta-analyses, continuous-dose BMI analyses tend to detect a weak risk increase, but categorical contrasts often attenuate the signal. Because more recent cohort studies show stronger associations than older ones, even with categorical BMI, further large-scale, well-adjusted studies are warranted. The overall study characteristics are shown in Table 3 . 2 , 16 , 36 , 47 , 49 , 50
Kidney cancer
Higher BMI is clearly associated with an increased risk of kidney cancer. A 2024 meta-analysis including four studies reported an RR of 1.50 (95% CI, 1.14 to 1.96) for BMI ≥25 kg/m 2 versus <23 kg/m 2 , with a similar magnitude in males and females. 4 The overall study characteristics are shown in Table 4 . 4 , 17 , 25 , 36 , 51 , 52
Thyroid cancer
Two meta-analyses published in 2024 reported divergent estimates of the thyroid cancer risk associated with BMI. One of them suggested an inverse association for BMI ≥30 kg/m 2 versus <25 kg/m 2 (RR, 0.72; 95% CI, 0.52 to 0.98), but it analyzed only two studies. 4 The other one, a larger synthesis of 27 studies, observed a positive association with BMI/weight (RR, 1.22; 95% CI, 1.14 to 1.30) and central adiposity measured by WC (RR, 1.12; 95% CI, 1.03 to 1.21). 53 Supporting that result, large-scale Korean cohort studies have also reported an increased thyroid cancer risk at higher BMI: ≥25 kg/m 2 versus <23 kg/m 2 (RR, 1.51; 95% CI, 1.35 to 1.78) 54 and ≥30 kg/m 2 versus <23 kg/m 2 (RR, 1.27; 95% CI, 1.05 to 1.55). 55
The overall pattern points to a modest positive association between thyroid cancer risk and higher BMI and central adiposity, but heterogeneity by the exposure definition and study design must be acknowledged. The overall study characteristics are shown in Table 4 . 4 , 17 , 25 , 53 - 57
Meningioma
Meta-analytic evidence indicates a clear positive association between meningioma and obesity. A 2025 meta-analysis of seven studies reported an increased risk for individuals with BMI ≥30 kg/m 2 versus <25 kg/m 2 (RR, 1.38; 95% CI, 1.16 to 1.64). For central adiposity (WC), the same analysis showed a stronger association (highest vs. lowest quantile: RR, 1.89; 95% CI, 1.34 to 2.66). 58 Overall, higher BMI and central adiposity are associated with a higher meningioma risk, and the effect for central adiposity is more pronounced. The overall study characteristics are shown in Table 4 . 58 - 62
Multiple myeloma
A 2019 meta-analysis pooling 12 male and 11 female study arms reported increased multiple myeloma risks associated with obesity (BMI ≥30 kg/m 2 vs. <25 kg/m 2 ): males RR 1.17 (95% CI, 1.01 to 1.34) and females RR 1.27 (95% CI, 1.15 to 1.40). 63 Recent cohort studies show mixed magnitudes: a pooled United States analysis reported a higher risk per 5 kg/m 2 BMI increase (RR, 1.17; 95% CI, 1.05 to 1.29), 64 but a Swedish cohort found no categorical association (RR, 1.12; 95% CI, 0.97 to 1.29). 20 Together, these data highlight heterogeneity by population and exposure modeling, despite an overall modest positive tendency. The overall study characteristics are shown in Table 4 . 17 , 20 , 25 , 63 - 66
EMERGING BUT INCONCLUSIVE EVIDENCE LINKING OBESITY AND CANCER RISK
In addition, there are other cancers for which evidence of an association with obesity is emerging but still controversial.
Oral cancer
Across the available studies, BMI shows little or no association, but central adiposity (WC) is positively associated with the risk of oral cancer. A pooled analysis of 20 cohorts reported no significant association per 5-kg/m 2 increase in BMI (RR, 1.10; 95% CI, 0.97 to 1.25) but a positive association per 5-cm increase in WC (RR, 1.09; 95% CI, 1.03 to 1.16). 67 These findings suggest that fat distribution, as captured by central adiposity, might be more informative than BMI for oral cancer risk. The overall study characteristics are shown in Table 5 . 16 , 17 , 67 , 68
Melanoma
The evidence suggests a sex-specific pattern. A global meta-analysis of 31 studies reported a higher melanoma risk among males with obesity (BMI ≥30 kg/m 2 vs. <25 kg/m 2 ; RR, 1.31; 95% CI, 1.19 to 1.44), but no association among females (RR, 0.99; 95% CI, 0.83 to 1.18). 69 Consistent with those meta-analytic findings, several cohort studies have shown a similar male-specific elevation with null findings in females. 17 , 20 Adding regional evidence, in a Korean study, melanoma risk increased according to obesity status: the adjusted hazard ratio (HR) for melanoma risk was 1.29 (95% CI, 1.07 to 1.557) in overweight individuals, 1.20 (95% CI, 1.00 to 1.44) in obese individuals, and 1.19 (95% CI, 0.80 to 1.78) in severely obese individuals, compared with individuals whose weight was within the recommended range. In stratified analyses, similar trends were observed in males and premenopausal, but not postmenopausal, females. 70 Taken together, these sex-specific patterns might be explained in part by residual confounding from ultraviolet exposure (sun-seeking behavior, outdoor work, holidays, tanning devices, exposed body surface area, and clothing patterns). The overall study characteristics are shown in Table 5 . 17 , 20 , 69 , 70
Bladder cancer
Evidence for an association between bladder cancer and BMI remains controversial, largely because of strong confounding by tobacco exposure. In a Korean cohort that performed smoking-stratified analyses, obesity (BMI ≥30 kg/m 2 vs. <23 kg/m 2 ) was associated with a modest increase in risk (RR, 1.17; 95% CI, 1.05 to 1.28). 71 However, the estimates diverge across cohorts: in a large Korean cohort, BMI-defined obesity was inversely associated with bladder cancer (BMI ≥30 kg/m 2 vs. <23 kg/m 2 ; RR, 0.84; 95% CI, 0.76 to 0.92), 51 whereas central adiposity remained positively associated after BMI adjustment (WC Q5 vs. Q1: RR, 1.38; 95% CI, 1.25 to 1.52). 17 Those discrepancies highlight the need for rigorous adjustment for smoking (status, pack-years, and cessation) and standardized definitions of obesity to clarify the independent effect of obesity on bladder cancer risk. The overall study characteristics are shown in Table 5 . 16 , 17 , 36 , 51 , 71
Prostate cancer
Current meta-analyses do not show a clear association between prostate cancer and BMI. A 2024 meta-analysis of five studies reported an RR of 0.97 (95% CI, 0.82 to 1.16) for BMI ≥30 kg/m 2 versus <25 kg/m 2 , 72 and another 2024 meta-analysis of six studies found an RR of 0.95 (95% CI, 0.91 to 0.99). 4
The largely null findings for overall incidence likely reflect detection bias: obese males tend to have lower prostate-specific antigen (PSA) concentrations than non-obese males and might undergo fewer biopsies, 73 leading to under-detection of indolent tumors. Nonetheless, obesity was associated with a higher risk of aggressive disease. In the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, in which nearly all biopsies were performed per protocol regardless of PSA level, obesity (BMI ≥30 kg/m 2 ) was associated with increased odds of high-grade prostate cancer (odds ratio, 1.28; 95% CI, 1.01 to 1.63). 74 The overall study characteristics are shown in Table 5 . 2 , 16 , 36 , 72 , 75
Non-Hodgkin lymphoma
Meta-analytic evidence indicates a modest positive association between obesity and non-Hodgkin lymphoma. A 2019 meta-analysis of 44 studies reported higher risks for obese individuals (BMI ≥30 kg/m 2 vs. <25 kg/m 2 : RR, 1.17; 95% CI, 1.06 to 1.28 in males; RR, 1.14; 95% CI, 1.05 to 1.24 in females) and small dose–response increases (per 5 kg/m 2 : RR, 1.05; 95% CI, 1.02 to 1.09 in males; RR, 1.04; 95% CI, 1.01 to 1.07 in females). 63 Overall, most of the included cohorts showed risk elevations of small magnitude. 16 , 25 The overall study characteristics are shown in Table 5 . 17 , 25 , 63
Leukemia
Meta-analytic evidence indicates a modest positive association between leukemia and a high BMI. A 2019 meta-analysis pooling 10 male and eight female study arms reported increased risks for obese individuals (BMI ≥30 kg/m 2 vs. <25 kg/m 2 : RR, 1.37; 95% CI, 1.19 to 1.59 in males; RR, 1.36; 95% CI, 1.12 to 1.66 in females) and small dose–response increases (per 5 kg/m 2 : RR, 1.12; 95% CI, 1.06 to 1.18 in males; RR, 1.14; 95% CI, 1.05 to 1.25 in females). 63 The overall study characteristics are shown in Table 5 . 17 , 25 , 63
Other cancers
In general, obesity (BMI‑defined) is not associated with an increased risk of lung, cervical, or testicular germ‑cell cancer. 47 , 76 , 77
OBESITY MANAGEMENT INTERVENTIONS AND CANCER RISK
Obesity is a major risk factor for multiple types of cancer, and the burden of obesity and obesity-related cancers on public health is substantial worldwide. 78 In this context, there is a growing need for obesity management interventions aimed at cancer prevention. Evidence-based obesity management strategies include lifestyle modifications (e.g., behavioral, nutritional, and exercise interventions), bariatric surgery, and pharmacotherapy. 78 - 82 Previous findings have demonstrated a lower risk of overall cancer or obesity-related cancers among patients who underwent obesity management interventions compared with obese control groups ( Table 6 ). 83 - 91
Intentional weight loss
A prospective cohort study found that obese postmenopausal females (BMI ≥30 kg/m 2 ) who achieved intentional weight loss had a significantly reduced risk of developing obesity-associated cancers (HR, 0.83; 95% CI, 0.71 to 0.99) compared with those who maintained a stable body weight, although the specific weight-loss methods used were not detailed ( Table 6 ). 92
Lifestyle and health behavior changes
In a systematic review and meta-analysis of 19 randomized clinical trials (RCTs), dietary interventions targeting weight loss, with or without exercise advice or programs, in adults with obesity (BMI ≥30 kg/m 2 ) and at least 1 year of follow-up did not significantly reduce the incidence of new cancers. However, that finding was based on evidence rated as low quality, limiting the strength of the conclusions (risk ratio, 0.92; 95% CI, 0.63 to 1.36). 91
Notably, a recent RCT (Look Action for Health in Diabetes [Look AHEAD] trial) conducted in the United States showed promising results for lifestyle management to reduce obesity-related cancer risk. It included overweight or obese adults (BMI >25 kg/m 2 ) with type 2 diabetes mellitus who received intensive lifestyle interventions (ILI): calorie restriction (1,200–1,800 kcal/day, with <30% of calories from fat and >15% from protein), meal-replacement products, and moderate-intensity physical activity (≥175 minutes/week). Although statistically insignificant, those in the study arm showed a trend toward a lower risk of obesity-related cancers (HR, 0.84; 95% CI, 0.64 to 1.04) compared with those in the control group, who attended group sessions that focused only on diet, exercise, and social support. On the other hand, the patients in the ILI group did not differ significantly from those in the control group in the risk of non-obesity-related cancers (HR, 1.02; 95% CI, 0.83 to 1.27) ( Table 6 ). 87
Pharmacologic therapy
Pharmacologic treatments are effective for obesity management, and the degree of weight-loss efficacy varies depending on the pharmacological mechanism of action. 80 Among those agents, glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have received increasing attention for not only promoting weight loss but also improving insulin sensitivity and exerting anti-inflammatory effects. 88 , 89 However, concerns have been raised about possible links between GLP-1 RAs and several cancers, 93 - 96 including thyroid cancer, 97 , 98 pancreatic cancer, 96 , 99 , 100 and CRC. 96 , 101 The evidence remains inconsistent, so here we examine and summarize studies that have investigated the association between GLP-1 RAs for obesity treatment and cancer risk.
A retrospective United States cohort study reported that GLP-1 RA (liraglutide, semaglutide, and dulaglutide) use was associated with a significantly reduced risk of several cancers: gastrointestinal cancer (HR, 0.67; 95% CI, 0.59 to 0.75), skin cancer (HR, 0.62; 95% CI, 0.55 to 0.70), breast cancer (HR, 0.72; 95% CI, 0.64 to 0.82), female genital cancers (HR, 0.61; 95% CI, 0.53 to 0.71), prostate cancer (HR, 0.68; 95% CI, 0.58 to 0.80), and lymphoid/hematopoietic cancers (HR, 0.69; 95% CI, 0.60 to 0.80). 88 In subgroup analyses of individual GLP-1 RA agents, the risk of gastrointestinal cancers was lower among patients treated with semaglutide (HR, 0.45; 95% CI, 0.37 to 0.53) than in non-users. However, liraglutide use was associated with increased risks of thyroid cancer (HR, 1.70; 95% CI, 1.03 to 2.82) and respiratory cancer (HR, 1.62; 95% CI, 1.13 to 2.32). 88
Another recent United States retrospective cohort study on the incidence of 13 obesity-related cancers and lung cancer found that GLP-1 RAs (liraglutide and semaglutide) and the dual gastric inhibitory polypeptide and GLP-1 RA tirzepatide were associated with a lower risk of overall cancer (HR, 0.83; 95% CI, 0.76 to 0.91), endometrial cancer (HR, 0.75; 95% CI, 0.57 to 0.99), ovarian cancer (HR, 0.53; 95% CI, 0.29 to 0.96), and meningioma (HR, 0.69; 95% CI, 0.48 to 0.97). 102
According to a recent meta-analysis of 50 RCTs (n=55,305 in the GLP-1 RA [liraglutide, semaglutide, exenatide, dulaglutide, and lixisenatide] group, n=47,467 in the control group) with a median study duration of 65 weeks, the risk of uterine cancer, which is an obesity-related cancer, was lower in the GLP-1 RA group (Mantel-Haenszel odds ratio [MH-OR], 0.24; 95% CI, 0.06 to 0.94) than the control group, but the overall cancer incidence did not differ significantly between the groups (MH-OR, 1.05; 95% CI, 0.98 to 1.13). However, GLP-1 RA users had higher risks for certain cancers that varied with the follow-up duration: thyroid cancer (MH-OR, 1.55; 95% CI, 1.05 to 2.27 for overall follow-up; MH-OR, 1.31; 95% CI, 0.68 to 2.52 for follow-up shorter than 104 weeks; MH-OR, 1.68; 95% CI, 1.05 to 2.70 for follow-up of 104 weeks or longer) and CRC (MH-OR, 1.27; 95% CI, 1.03 to 1.57 for overall follow-up; MH-OR, 2.28; 95% CI, 1.04 to 4.98 for follow-up shorter than 104 weeks; MH-OR, 1.20; 95% CI, 0.96 to 1.50 for follow-up of 104 weeks or longer). 89 The increased incidence of CRC could also be attributed to diagnostic workup for gastrointestinal side effects caused by GLP-1 RAs. Further large-scale trials with longer follow-up are warranted to clarify the effects of these weight loss medications on obesity-associated cancer risk ( Table 6 ).
Bariatric surgery
A recent meta-analysis of 32 cohort studies involving patients with morbid obesity (n=511,585 in the bariatric surgery group, n=1,889,746 in the control group) demonstrated a reduced risk of overall (RR, 0.62; 95% CI, 0.46 to 0.84) and obesity-related cancers (RR, 0.59; 95% CI, 0.39 to 0.90) following bariatric surgery. The risk of specific cancers varied by cancer type (hepatocellular carcinoma [RR, 0.35; 95% CI, 0.22 to 0.55], CRC [RR, 0.63; 95% CI, 0.50 to 0.81], pancreatic cancer [RR, 0.52; 95% CI, 0.29 to 0.93], gallbladder cancer [RR, 0.41; 95% CI, 0.18 to 0.96], breast cancer [RR, 0.56; 95% CI, 0.44 to 0.71], endometrial cancer [RR, 0.38; 95% CI, 0.26 to 0.55], and ovarian cancer [RR, 0.45; 95% CI, 0.31 to 0.64]). However, no significant risk reduction was observed for esophageal, gastric, thyroid, kidney, or prostate cancer. 86 The relatively short follow-up duration and a young patient population (mean age mid-40s) may result in an underestimation of esophageal and prostate cancer incidence following bariatric surgery, as these cancers typically develop later in life with a prolonged latency period. 103 For gastric cancer, most studies did not differentiate between cardia and non-cardia subtypes, limiting precise risk assessment. Some studies report that the association between obesity and gastric cancer differs according to the tumor location. 104 Additionally, biases such as surveillance and selection bias, and lack of adjustment for confounders such as comorbidities, smoking, and alcohol use may further complicate the interpretation of nonsignificant findings. 86
Bariatric surgery was also associated with a lower incidence of cancer in the long term. According to a retrospective cohort study conducted in the United States, obese patients (BMI ≥35 kg/m 2 ) who underwent bariatric surgery showed a significantly lower 10-year incidence of obesity-related cancers (HR, 0.48; 95% CI, 0.46 to 0.51) than those who did not undergo surgery. 83 Site-specific analyses showed reduced risks for breast (HR, 0.75; 95% CI, 0.68 to 0.84), colon (HR, 0.64; 95% CI, 0.54 to 0.75), liver (HR, 0.37; 95% CI, 0.35 to 0.40), ovary (HR, 0.65; 95% CI, 0.53 to 0.81), and endometrial (HR, 0.45; 95% CI, 0.36 to 0.56) cancers. 83
In a Nordic retrospective cohort study of older adults (≥60 years) with obesity, patients who underwent gastric bypass surgery, which induces profound weight loss, had a lower risk of obesity-related cancers (HR, 0.74; 95% CI, 0.56 to 0.97) ( Table 6 ). 85
Taken together, the results of previous studies suggest that obesity management strategies—lifestyle modifications, bariatric surgery, and pharmacologic therapy—might reduce cancer incidence in individuals with obesity. 83 - 90 A comprehensive, multimodal preventive approach appears essential for cancer risk reduction in this population. Further well-designed randomized controlled trials with adequate follow-up durations are warranted to confirm and strengthen the evidence that obesity management has preventive effects against cancer incidence.
CONCLUSION
Obesity is linked to a higher incidence of all the NCI-designated obesity-associated cancers, with effect sizes varying by histology, subsite, sex or menopause, and adiposity metric (central adiposity often exceeds BMI). Intentional weight loss via lifestyle change, pharmacotherapy, or bariatric surgery appears to reduce the overall and site-specific cancer risks, though estimates remain heterogeneous.
A multimodal prevention strategy and rigorously designed, adequately powered studies are needed to confirm and refine these associations.
ACKNOWLEDGMENTS
This study was fully supported by a grant from the Korean Foundation for Cancer Research (KFCR) (grant number: CB-2022-A-1).
CONFLICTS OF INTEREST
The authors declare no conflict of interest.
AUTHOR CONTRIBUTIONS
Study concept and design: JL, SK, IYC, and DWS; Acquisition of data: JL and SK; analysis and interpretation of data: JL and SK; drafting of the manuscript: JL and SK; critical revision of the manuscript: JL, SK, IYC, and DWS; and study supervision: DWS.
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