In the early 1980s, Doll and Peto estimated that about 35% of all deaths from cancer in the United States were attributable to dietary factors, with a margin of uncertainty ranging from 10 to 70%. Since then, several dietary factors, e.g. fat and meat, have been suggested to increase the risk for cancer, while other factors, e.g. fibre, fruit and vegetables, have been suggested to decrease the risk. The case-control and cohort studies have, however, given ambiguous results, and the overall evidence is far from conclusive. The major findings on dietary factors that increase risk have been reported from case-control studies, but have not been confirmed in large population-based cohort studies. Although the research in this area indicates that diet is important in cancer prevention, current knowledge does not allow reliable estimates of the numbers and proportions of cancers that could be avoided through well-described modifications of dietary habits. During the last 10 years, low physical activity has been pinpointed as a risk factor for cancers at various sites, especially the colon; however, the causal mechanism is still unknown. Obesity, defined as a body mass index of 30 or more, is consistently associated with endometrial and gall-bladder cancers in women and renal-cell cancer in both men and women. As the prevalence of obesity was between 5 and almost 20% in the Nordic populations in 1995, 625 cancer cases (310 endometrial cancers, 270 renal-cell cancers in men and women and 45 gall-bladder and bile-duct cancers among women) can be predicted in the Nordic countries around the year 2000 to be caused by obesity. This implies that about 1% of all cancers in Nordic women and less than 1% of those in Nordic men could be avoided around the year 2000 if a healthy body weight could be maintained by all inhabitants.
The role of diet in the aetiology of renal cell carcinoma was investigated in a population-based case-control study in Denmark. Cases were 20-79 years old, with a histologically verified diagnosis of renal cell carcinoma. Controls were sampled from the general population and were frequency-matched on age and sex. A total of 351 cases (73% of the eligible) and 340 controls (68% of the eligible) were included in the study. Dietary information was obtained in a self-administered food frequency questionnaire and the information was confirmed in a subsequent interview performed by trained interviewers who also elicited information on other suspected risk factors such as smoking, occupation, medical history, education and reproductive history. Logistic regression models were used to calculate the odds ratios, and, both frequency of consumption of various food stuffs and computed nutrients were examined. A positive association was observed between risk of renal cell carcinoma and total energy intake (odds ratio, OR, for highest quartile compared to lowest: 1.7 (95% confidence interval, CI, 1.0-3.0) for men, and 3.5 (95% CI 1.6-6.5) for women), fat intake (OR for highest quartile compared to lowest: 1.9 (95% CI 1.1-3.5) for men, and 3.3 (95% CI 1.6-6.9) for women). For women, an effect was also seen for intake of carbohydrates (OR for highest quartile compared to lowest: 3.2 (95% CI 1.5-6.8), while no protective effect was seen for vegetables or fruit. Dairy products may be associated with risk of renal cell cancer (OR for women using thickly spread butter compared to thinly spread: 11.4 (95% CI 2.8-45), OR for women who drank more than one glass of milk with 3.5% fat content compared to never drink milk: 3.7 (95% CI 1.2-11). As expected, total energy intake, intake of fat, protein and carbohydrates were closely correlated making it difficult to identify one of the energy sources as more closely associated with risk of renal cell cancer than the other. Several energy sources have been identified as possible risk factors for renal cell carcinoma. It is possible that a high energy intake as such rather than the individual sources are responsible for the increased risk. Furthermore, dairy fats may be associated with renal cell carcinoma risk. The observed associations appeared stronger in women, and did not explain the association with obesity and low socio-economic status previously found in Denmark.
Follow-up studies have suggested that total intake of trans fatty acids (TFA) is a risk factor for gain in body weight and waist circumference (WC). However, in a cross-sectional study individual TFA isomers in adipose tissue had divergent associations with anthropometry. Our objective was to investigate the association between intake of TFA from ruminant dairy and meat products and subsequent changes in weight and WC. Furthermore, potential effect modification by sex, age, body mass index and WC at baseline was investigated.
Data on weight, WC, habitual diet and lifestyle were collected at baseline in a Danish cohort of 30,851 men and women aged 50-64 years. Follow-up information on weight and WC was collected 5 years after enrolment. The associations between intake of ruminant TFA (R-TFA) and changes in weight and WC were analysed using multiple linear regression with cubic spline modelling.
Intake of R-TFA, both absolute and energy-adjusted intake, was significantly associated with weight change. Inverse associations were observed at lower intakes with a levelling-off at intakes >1.2?g/day and 0.4 energy percentage (E %). Absolute, but not energy-adjusted, intake of R-TFA was significantly associated with WC change. An inverse association was observed at lower intakes with a plateau above an intake of 1.2?g/day.
The present study suggests that intake of R-TFA is weakly inversely associated with changes in weight, whereas no substantial association with changes in WC was found.