Giuseppe Preziosi1, Jude A Oben2, Giuseppe Fusai3. 1. Hepato-Pancreatico-Biliary Surgery and Liver Transplant Unit, Royal Free Hospital, London, United Kingdom. Electronic address: g.preziosi@ucl.ac.uk. 2. Centre for Liver and Digestive Health, University College London, Royal Free Hospital, London, United Kingdom. 3. Hepato-Pancreatico-Biliary Surgery and Liver Transplant Unit, Royal Free Hospital, London, United Kingdom.
Abstract
BACKGROUND: Pancreatic cancer is an invariably fatal malignancy. Cigarette smoking and diabetes are established risk factors, but over the last two decades studies have shown that excess adiposity is an additional independent risk factor with 30-50% of cases thought to be attributed to nutritional factors. The aim of this narrative review is to analyze all the epidemiological evidence on the topic and possible pathophysiology. METHODS: We searched PubMed, Embase, Cochrane Library and Medline, and all available evidence was included. We firstly analyze meta- and pooled analysis. Then we discuss individual studies to identify sources of discrepancies between studies and attempt to delineate pathophysiology. RESULTS: It is estimated that obese individuals have a relative risk (RR) ranging between 1.19 and 1.47, when compared with those of normal weight, regardless of diabetes or smoking status. No significant differences were found between gender. CONCLUSION: There is a measurable increased risk of developing pancreatic cancer in obese individuals, and excess adiposity is related to the condition with a "dose-response" curve. Hyperinsulinemia and possibly hyperestrogenism secondary to a metabolic syndrome, and independently from diabetes status, appear to be the key elements of the pathogenesis in pancreatic cancer secondary to excess body fat. Increased efforts should therefore be made in tackling the epidemic levels of obesity in the Western world countries.
BACKGROUND:Pancreatic cancer is an invariably fatal malignancy. Cigarette smoking and diabetes are established risk factors, but over the last two decades studies have shown that excess adiposity is an additional independent risk factor with 30-50% of cases thought to be attributed to nutritional factors. The aim of this narrative review is to analyze all the epidemiological evidence on the topic and possible pathophysiology. METHODS: We searched PubMed, Embase, Cochrane Library and Medline, and all available evidence was included. We firstly analyze meta- and pooled analysis. Then we discuss individual studies to identify sources of discrepancies between studies and attempt to delineate pathophysiology. RESULTS: It is estimated that obese individuals have a relative risk (RR) ranging between 1.19 and 1.47, when compared with those of normal weight, regardless of diabetes or smoking status. No significant differences were found between gender. CONCLUSION: There is a measurable increased risk of developing pancreatic cancer in obese individuals, and excess adiposity is related to the condition with a "dose-response" curve. Hyperinsulinemia and possibly hyperestrogenism secondary to a metabolic syndrome, and independently from diabetes status, appear to be the key elements of the pathogenesis in pancreatic cancer secondary to excess body fat. Increased efforts should therefore be made in tackling the epidemic levels of obesity in the Western world countries.
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