Reflections on the latest findings on pancreatic cancer
In June 2012 the Continuous Update Project (CUP) Panel, of which I am a member, met in London to discuss the updated evidence for associations between food, nutrition, physical activity and the risk of pancreatic cancer. Since the last review for the Second Expert Report in 2007 a further 79 articles from cohort studies or randomised controlled trials have been added to the CUP database bringing the total number for this cancer to 208 and providing us with a tranche of new evidence to assess.
A large proportion of the evidence comes from cohort studies examining measures of body fatness, and pancreatic cancer. We decided to combine several exposures relating to body fatness, (body fatness, abdominal fatness, weight gain), which allowed the Panel to draw a single conclusion. The evidence suggested that body fatness was important in different population groups and for men and women.
This new evidence has served to strengthen and confirm the judgements made by the Expert Panel for the 2007 Second Expert Report that body fatness is a convincing cause of pancreatic cancer. Given the accumulating evidence that body fatness increases the risk of other cancers, the clear message must be that maintaining body weight within the normal range lowers cancer risk.
In the 2007 Report ‘adult attained height’ was also judged as probably increasing risk of pancreatic cancer. Since then more cohort studies have been published and the evidence base has increased. However, the CUP Panel considered that the updated evidence did not justify changing the conclusions drawn in the 2007 Report. There are more cohort studies showing a positive association between adult attained height and pancreatic cancer risk but there was sufficient inconsistency between studies to prevent upgrading the evidence from probable.
Adult height is a marker of different aspects of growth in childhood, including growth in length and acquisition of body fat, and the exposure has been defined as ‘greater childhood growth’ but we need more evidence to work out exactly what it means.
Consideration was also given to new evidence for dietary constituents, including red and processed meat, alcohol, and foods and drinks containing fructose or saturated fat. The updated evidence for consumption of each of these dietary constituents was judged suggestive of an associated increased risk of pancreatic cancer. The evidence linking fructose intake with pancreatic cancer is intriguing; however the lack of concordance with effects of exposure to sucrose is surprising. It was also noted that the evidence for fructose rested on studies only from USA, so there is uncertainty about applicability to other populations, and the Panel agreed that further studies are needed.
The CUP update for pancreatic cancer constitutes the most up-to-date assessment of the role of food, nutrition, physical activity and body weight for prevention of pancreatic cancer and provides us with a robust evidence base on which to make recommendations for cancer prevention.