Serum Lipids and the Risk of Gastrointestinal Malignancies in the Swedish AMORIS Study

Background. Metabolic syndrome has been linked to an increased cancer risk, but the role of dyslipidaemia in gastrointestinal malignancies is unclear. We aimed to assess the risk of oesophageal, stomach, colon, and rectal cancers using serum levels of lipid components. Methods. From the Swedish Apolipoprotein Mortality Risk (AMORIS) study, we selected 540,309 participants (>？20 years old) with baseline measurements of total cholesterol (TC), triglycerides (TG), and glucose of whom 84,774 had baseline LDL cholesterol (LDL), HDL cholesterol (HDL), apolipoprotein B (apoB), and apolipoprotein A-I (apoA-I). Multivariate Cox proportional hazards regression was used to assess glucose and lipid components in relation to oesophageal, stomach, colon, and rectal cancer risk. Results. An increased risk of oesophageal cancer was observed in persons with high TG (e.g. HR: 2.29 (95% CI: 1.42–3.68) for the 4th quartile compared to the 1st) and low LDL, LDL/HDL ratio, TC/HDL ratio, log (TG/HDL), and apoB/apoA-I ratio. High glucose and TG were linked with an increased colon cancer risk, while high TC levels were associated with an increased rectal cancer risk. Conclusion. The persistent link between TC and rectal cancer risk as well as between TG and oesophageal and colon cancer risk in normoglycaemic individuals may imply their substantiality in gastrointestinal carcinogenesis. 1. Introduction The prevalence of dyslipidaemia is increasing worldwide [1, 2], either alone or as part of the metabolic syndrome [3]. Many epidemiological studies have consistently linked the metabolic syndrome as well as its separated components, most importantly impaired glucose metabolism and obesity, with increased risk of cancer [4–6]. However, the association between abnormal levels of serum lipid components as the main features of dyslipidaemia and the risk of individual cancers is unclear. For gastrointestinal malignancies, a positive linear association has been reported between triglycerides (TG) and risk of colon and rectal cancer [7–9]. In contrast, the role of total cholesterol (TC) in oesophageal, stomach, colon, and rectal cancer development remains inconsistent in observational studies [9–11]. Little is known about how other specific lipid markers such as high-density lipoprotein cholesterol (HDL) and low-density lipoprotein cholesterol (LDL) and their components, apolipoprotein A-I (apoA-I) and apolipoprotein B (apoB), affect cancer risk [12, 13]. To date, the precise mechanism by which serum lipids contribute to the development of cancer is unknown. Dyslipidaemia enhances