Excess body weight and the risk of primary liver cancer: An updated meta-analysis of prospective studies

Chen, Yi; Wang, Xiaolin; Wang, Jianhua; Zhang, Yan; Luo, Jianjun

doi:10.1016/j.ejca.2012.02.063

Cited by 208 publications

(144 citation statements)

References 61 publications

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“…3 Calibrated data were obtained by linear regression models that compared observed nutrient questionnaire measurements with 24-hr dietary recall. 4 Stratified by age (1-yearearear intervals), sex and center, and adjusted for baseline alcohol intake (g/day; continuous) and non-alcohol total energy intake (kcal/day; continuous).…”

Section: Discussionmentioning

confidence: 99%

“…[2][3][4][5][6] A substantial proportion of the steadily increasing incidence of HCC is in high and middle income countries 7 and is more likely to occur in persons without apparent exposure to aflatoxins, or HBV/HCV, suggesting a need for greater emphasis on other modifiable risk factors, particularly those related to diet and lifestyle. 7,8 Western-type diets are characterized by a relatively higher proportion of fats, but the impact of dietary fat and its main subtypes on HCC risk has not been well explored.…”

Section: What's New?mentioning

confidence: 99%

“…3 No information on past alcohol consumption (defined in the Supporting Information) was available for the following EPIC centres: Naples, Bilthoven, Umeå , Malm€ o, and Norway. 4 All dietary variables were adjusted for non-alcohol energy by residual method, except for energy, coffee and alcohol intake. …”

Section: Nested Case-control Studymentioning

confidence: 99%

“…3 Calibrated data were obtained by linear regression models that compared observed nutrient questionnaire measurements with 24-h dietary recall. 4 Stratified by age (1-yearearear intervals), sex and center, and adjusted for baseline alcohol intake (g/day; continuous) and non-alcohol total energy intake (kcal/day; continuous). 5 Additionally adjusted for sex-specific physical activity level (inactive, moderately inactive, moderately active, active, and missing), body mass index (kg/m 2 ; continuous), smoking status (never, former, current, unknown), self-reported diabetes status (yes, no, unknown), lifetime alcohol intake pattern (never drinkers, former light drinker, former heavy drinkers, light drinkers, never heavy drinkers, periodically heavy drinkers, always heavy drinkers, unknown), coffee intake (ml/d; continuous), and intake of dietary fiber (g/day).…”

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confidence: 99%

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Dietary fat, fat subtypes and hepatocellular carcinoma in a large European cohort

Duarte‐Salles

Fedirko

Stępień

et al. 2015

Intl Journal of Cancer

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The role of amount and type of dietary fat consumption in the etiology of hepatocellular carcinoma (HCC) is poorly understood, despite suggestive biological plausibility. The associations of total fat, fat subtypes and fat sources with HCC incidence were investigated in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, which includes 191 incident HCC cases diagnosed between 1992 and 2010. Diet was assessed by country-specific, validated dietary questionnaires. A single 24-hr diet recall from a cohort subsample was used for measurement error calibration. Hazard ratios (HR) and 95% confidence intervals (95% CI) were estimated from Cox proportional hazard models. Hepatitis B and C viruses (HBV/HCV) status and biomarkers of liver function were assessed separately in a nested case–control subset with available blood samples (HCC = 122). In multivariable calibrated models, there was a statistically significant inverse association between total fat intake and risk of HCC (per 10 g/day, HR = 0.80, 95% CI: 0.65–0.99), which was mainly driven by monounsaturated fats (per 5 g/day, HR = 0.71, 95% CI: 0.55–0.92) rather than polyunsaturated fats (per 5 g/day, HR = 0.92, 95% CI: 0.68–1.25). There was no association between saturated fats (HR = 1.08, 95% CI: 0.88–1.34) and HCC risk. The ratio of polyunsaturated/monounsaturated fats to saturated fats was not significantly associated with HCC risk (per 0.2 point, HR = 0.86, 95% CI: 0.73–1.01). Restriction of analyses to HBV/HCV free participants or adjustment for liver function did not substantially alter the findings. In this large prospective European cohort, higher consumption of monounsaturated fats is associated with lower HCC risk

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Section: Discussionmentioning

confidence: 99%

Section: What's New?mentioning

confidence: 99%

Section: Nested Case-control Studymentioning

confidence: 99%

mentioning

confidence: 99%

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Dietary fat, fat subtypes and hepatocellular carcinoma in a large European cohort

Duarte‐Salles

Fedirko

Stępień

et al. 2015

Intl Journal of Cancer

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“…The WCRF has found conclusive evidence that links liver cancer to excess adiposity, and substantial evidence has been accumulated in recent years to support that conclusion (Wang et al 2012b, Chen et al 2012, Chen et al 2013, Schlesinger et al 2013, World Cancer Research Fund International 2015. Clearly, chronic viral infection in the liver is the leading cause of liver cancer, but any other factors that also cause hepatocellular injury and hepatocellular proliferation, including alcohol use, chronic exposure to other chemicals, and excess adiposity, can increase risk.…”

Section: Liver Cancermentioning

confidence: 99%

Body fatness as a cause of cancer: epidemiologic clues to biologic mechanisms

Byers¹,

Sedjo²

2015

Endocrine-Related Cancer

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Carrying excess body fat is a leading cause of cancer. Epidemiologic evidence gives strong clues about the mechanisms that link excess adiposity to risk for several cancer sites. For postmenopausal breast cancer and endometrial cancer, the hyper-estrogenic state that is induced by excess body fatness is the likely cause. For esophageal cancer and gallbladder cancer, chronic local inflammation induced by acid reflux and gallstones is the likely cause, and for liver cancer, local inflammation induced by hepatic fatty infiltration is the likely cause. However, for several other cancers known to be associated with excess adiposity, including cancers of the colon, pancreas, ovary, kidney, and prostate, specific causes are not known. Possible candidates include elevated systemic or local tissue inflammation induced by adiposity and effects of the elevated levels of leptin, insulin, IGFs, and depressed immune function that are seen with excess adiposity. There is growing evidence that intentional weight loss not only reduces circulating levels of cancer-associated factors but that it also reduces cancer incidence and recurrence. Better research is needed to understand the mechanisms that link excess body fat to cancer risk as well as to understand the amount of weight loss needed for substantial cancer risk reduction. Finally, as we develop better understanding of the mediators of the effects of excess body fatness on cancer risk, we should identify pharmacologic interventions that target those mediators so that they can be used to complement weight loss in order to reduce cancer risk.

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Association of High Body Mass Index and Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Virus Infection

2018

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Excess body weight and the risk of primary liver cancer: An updated meta-analysis of prospective studies

Cited by 208 publications

References 61 publications

Dietary fat, fat subtypes and hepatocellular carcinoma in a large European cohort

Dietary fat, fat subtypes and hepatocellular carcinoma in a large European cohort

Body fatness as a cause of cancer: epidemiologic clues to biologic mechanisms

Association of High Body Mass Index and Hepatocellular Carcinoma in Patients With Chronic Hepatitis B Virus Infection

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