Director's Update: October 19, 2004
The obesity epidemic has generated intense concern in the medical community, and rightfully so. It has had devastating consequences for our nation's health and health care system, driving rates of several chronic illnesses into the stratosphere and heaping tens of billions of dollars onto an already strained health care budget. And as we are beginning to better appreciate, obesity has also significantly affected cancer incidence, progression, and death rates. In fact, the most recent estimates attribute 3.2 percent of all new cancers - 14 percent of cancer deaths in men and 20 percent in women - to obesity.
NCI, on its own and in partnership with other HHS agencies, is focused on better understanding the link between obesity and cancer and, at the same time, working to minimize the epidemic's impact. We are also beginning to better understand that the influence of diet on cancer goes well beyond questions of quantity and energy expenditure.
To be sure, the food we eat every day is remarkably complex. Its nutrients and molecules have profound genetic and cellular effects that directly influence cancer susceptibility. The components of our daily diet - the calcium in milk, the zinc in chicken and nuts, the flavonoids in onions and carrots, the fatty acids in tuna or avocados - all alter a broad array of cancer-related events, including inflammatory response, carcinogen metabolism, cell death, and DNA repair.
The Nutrition Sciences Research Group (NSRG) in the NCI Division of Cancer Prevention, led by Dr. John A. Milner, is an important leader in this field of investigation, conducting and funding research aimed at detailing and further characterizing the delicate relationship between diet and cancer. We are becoming increasingly aware, for example, that genetics can affect the function of bioactive food components. Epidemiologic studies have shown that in patients with specific genetic polymorphisms that influence chromosomal stability, adequate levels of folate - a component of leafy vegetables and a nutrient often used to fortify processed foods such as breakfast cereals - likely decreases the risk of colorectal cancer. To further investigate the link between and colorectal cancer, NCI is funding a number of studies, including an effort being led by investigators at Harvard, Dartmouth, and Tufts by Dr. David J. Hunter to further elucidate the pathways through which folate may affect colorectal cancer risk and the influences of specific genetic mutations in determining that risk.
Importantly, some of the advanced technologies we are using in many areas of cancer research - including microarray analysis, nanotechnology, metabolomics, proteomics, and bioinformatics - may provide nutritional scientists with some valuable new tools, allowing them to identify molecular sites of action of bioactive food components, diagnose a person's nutritional status, and mine the flood of genomic data now available to more quickly identify those foods and compounds with the greatest cancer prevention properties.
However, each one of us is unique and has slight genetic variations: That means some of us respond to certain bioactive food components and some don't. As Dr. Milner stresses in his talks and published papers, our challenge is to ensure that we communicate the importance of collecting the genomic data needed to make understanding these differences a reality.
I'm confident this work will go a long way toward identifying appropriate dietary intervention strategies to reduce the risk of developing cancer and perhaps even change the behavior of existing malignant cells. Armed with a greater understanding of how obesity and diet influence cancer risk, we can look to a day where diet fads and crazes are supplanted by rational, evidence-based recommendations that promote true health and wellness.
Dr. Andrew C. von Eschenbach
Director, National Cancer Institute
|
