Background: Body mass index (BMI) is an established risk factor for colon cancer, but risks may differ between genders and colon subsites. Moreover, whether weight change influences risk is not yet clarified. We investigated these issues in a large, Norwegian, population-based cohort study.Methods: Participants' weight was measured at examinations up to three times between 1974 and 1988. Hazard ratios (HR) and confidence intervals (CI) were estimated using Cox regression.Results: During follow-up of 38,822 men and 37,357 women, we identified 228 proximal and 174 distal colon cancer cases in men and 237 and 159 cases, respectively, in women. The association between BMI and colon cancer risk differed between subsites in men (P = 0.02) but not in women (P = 0.95). In men, HRs (95% CIs) per 5 kg/m 2 were 1.07 (0.86-1.33) and 1.49 (1.19-1.87) for proximal and distal colon, respec-

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Intake of trans fatty acids (TFA) may influence systemic inflammation, insulin resistance and adiposity, but whether TFA intake influences cancer risk is insufficiently studied. We examined the association between TFA intake from partially hydrogenated vegetable oils (PHVO-TFA), partially hydrogenated fish oils (PHFO-TFA), and ruminant fat (rTFA) and cancer risk in the Norwegian counties study, a large cohort study with a participation rate >80%. TFA intake was assessed three times in 1974-1988 by questionnaire. A total of 77,568 men and women were followed up through 2007, during which time 12,004 cancer cases occurred. Hazard ratios (HRs) and confidence intervals (CIs) were estimated with Cox regression for cancer sites with !150 cases during follow-up. Significantly increased or decreased risks were found when comparing the highest and lowest intake categories (HRs, 95% CIs) for PHVO-TFA and pancreatic cancer in men (0.52, 0.31-0.87) and non-Hodgkin lymphoma (NHL) in both genders (0.70, 0.50-0.98); PHFO-TFA and rectal cancer (1.43, 1.09-1.88), prostate cancer (0.82, 0.69-0.96), and multiple myeloma (2.02, 1.24-3.28); and rTFA and all cancers (1.09, 1.02-1.16), cancer of the mouth/pharynx (1.59, 1.08-2.35), NHL (1.47, 1.06-2.04) and multiple myeloma (0.45, 0.24-0.84). Furthermore, positive trends were found for PHFO-TFA and stomach cancer (p trend 5 0.01) and rTFA and postmenopausal breast cancer (p trend 5 0.03). Inverse trends were found for PHVO-TFA and all cancers (p trend 5 0.006) and cancer of the central nervous system in women (p trend 5 0.005). PHFO-TFA, but not PHVO-TFA, seemed to increase cancer risk. The increased risks observed for rTFA may be linked to saturated fat.

Trans-fatty acids (TFA) have adverse effects on blood lipids, but whether TFA from different sources are associated with risk of CVD remains unresolved. The objective of the present study was to evaluate the association between TFA intake from partially hydrogenated vegetable oils (PHVO), partially hydrogenated fish oils (PHFO) and ruminant fat (rTFA) and risks of death of CVD, CHD, cerebrovascular diseases and sudden death in the Norwegian Counties Study, a population-based cohort study. Between 1974 and 1988, participants were examined for up to three times. Fat intake was assessed with a semi-quantitative FFQ. A total of 71 464 men and women were followed up through 2007. Hazard ratios (HR) and 95 % CI were estimated with Cox regression. Energy from TFA was compared to energy from all other sources, carbohydrates or unsaturated cis-fatty acids with different multivariable models. During follow-up, 3870 subjects died of CVD, 2383 of CHD, 732 of cerebrovascular diseases and 243 of sudden death. Significant risks, comparing highest to lowest intake category, were found for: TFA from PHVO and CHD (HR 1·23 (95 % CI 1·00, 1·50)) and cerebrovascular diseases (HR 0·65 (95 % CI 0·45, 0·94)); TFA from PHFO and CVD (HR 1·14 (95 % CI 1·03, 1·26)) and cerebrovascular diseases (HR 1·32 (95 % CI 1·04, 1·69)); and rTFA intake and CVD (HR 1·30 (95 % CI 1·05, 1·61)), CHD (HR 1·50 (95 % CI 1·11, 2·03)) and sudden death (HR 2·73 (95 % CI 1·19, 6·25)) in women. These associations with rTFA intake were not significant in men (P interaction $ 0·01). The present study supports that TFA intake, irrespective of source, increases CVD risk. Whether TFA from PHVO decreases risk of cerebrovascular diseases warrants further investigation.