Components of the metabolic syndrome and colorectal cancer risk; a prospective study

Abstract

Objective: To examine the relation of well-known factors of the metabolic syndrome (MetS) as well as related circulating factors, with risk of colorectal cancer. Methods: We performed a case control study of 306 colorectal cancer cases and 595 matched controls nested in the Northern Sweden Health and Disease Cohort. Levels of C-peptide, glycated haemoglobin (HbA1c), leptin and adiponectin were measured in cryopreserved samples. Body mass index (BMI), systolic and diastolic blood pressure and fasting and post-load plasma glucose, had been measured in a subcohort. Conditional logistic regression was used to calculate odds ratios (OR) of disease, including risk assessments for the MetS factors: obesity (BMI430 kg m À2 ), hypertension (blood pressure X140/90 mmHg or use of anti-hypertensive drugs) and hyperglycaemia (fasting glucose X6.1 mmol l À1 or post-load glucose in capillary plasma X8.9 mmol l À1 ). Results: None of the studied variables were significantly associated with risk across quartiles. Presence of obesity, hypertension and hyperglycaemia significantly increased the risk of colorectal cancer; OR for three vs null factors was 2.57 (95% Confidence Interval [CI] 1.20-5.52; P trend ¼ 0.0021), as compared to a 30 to 70% increased risk for the factors in single. Similarly, top decile levels of C-peptide, HbA1c and leptin/adiponectin ratio were associated with an increased risk; ORs for top vs deciles 1-9 were 1.56 (95% CI 0.93-2.62; P ¼ 0.090), 1.83 (95% CI 1.00-3.36; P ¼ 0.051) and 1.50 (95% CI 0.83-2.71; P ¼ 0.18), respectively. Conclusions: Our study support the view that components of the MetS increase risk of colorectal cancer, and further suggests that only very high levels of metabolic factors confer an increased risk.

Glycosylated Hemoglobin and Risk of Colorectal Cancer in Men and Women, the European Prospective Investigation into Cancer and Nutrition

“…Norway was not included in the current study because blood samples were only recently collected and very few colorectal cancer cases have occurred after blood donation. Sweden was not included because an independent study of HbA1c and colorectal cancer risk has already been undertaken (15).…”

“…A study based on Swedish populations showed a direct association of HbA1c with colorectal cancer risk only at very high concentrations (top decile levels; ref. 15). Most of these studies had a relatively small sample size (between 67 and 380 case subjects); thus, only a few studies allowed investigation into the role of HbA1c in colon and rectal cancers separately (15,22,23), and when this was the case, sample size and statistical power were generally limited.…”

“…15). Most of these studies had a relatively small sample size (between 67 and 380 case subjects); thus, only a few studies allowed investigation into the role of HbA1c in colon and rectal cancers separately (15,22,23), and when this was the case, sample size and statistical power were generally limited. The majority of these studies included only women (21,22,24), mainly from North American populations (21)(22)(23)(24).…”

“…Although diabetes has been repeatedly associated with an increase in colorectal cancer risk (11)(12)(13), less is known about the influence of hyperglycemia on the disease among nondiabetics. Only a few epidemiologic studies have investigated the relationship of blood glucose levels with colorectal adenoma and cancer incidence (6,14,15) or colorectal cancer mortality (16,17), but all of these suggested an implication of elevated blood glucose in the etiology of the disease.…”

Obesity and Obese-related Chronic Low-grade Inflammation in Promotion of Colorectal Cancer Development

“…Tamakoshi et al (2005) reported that invasiveness of CRC in women is associated with a high level of leptin in serum. It is suggested that only very high levels of leptin and other metabolic factors acting simultaneously (levels of C-peptide, HbA1c, and leptin/ObR ratio) activate and increase CRC proliferation (Stocks et al, 2008).…”