The accredited CME learning activity based on this article is offered under the auspices of the CE department of the University of Toronto. Participating physicians are entitled to one (1) MAINPRO-M1 credit by completing this program, found online at www.geriatricsandaging.ca/cme

Susan J. Whiting, PhD, College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK.
Hassanali Vatanparast, MD, College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, SK.

This review describes the current state of knowledge in nutritional interventions in osteoporosis, using the Osteoporosis Society of Canada’s (OSC) 2002 clinical practice guidelines for the diagnosis and management of osteoporosis as a basis. Nutrients important for osteoporosis are calcium, vitamin D, protein, sodium, caffeine, and isoflavones. These recommendations are updated and other nutrients and food components, not covered in the OSC 2002 report, are described. As a single nutrient approach is no longer warranted, we discuss how the Dietary Approaches to Stop Hypertension (DASH) diet can be used to provide appropriate intakes of many key nutrients for persons with, or at risk of, osteoporosis.
Key words: DASH diet, calcium, vitamin D, protein, osteoporosis.

A major study by the research group of Dr. Josef Penninger, at the University of Toronto, has identified a protein that, when absent, appears to contribute to the development of colorectal cancer. The protein in question is the p110g catalytic subunit of phosphoinositide-3-OH kinases (PI(3)Ks), a family of proteins that regulate a vast array of fundamental cell responses, including proliferation, transformation, differentiation and protection from apoptosis. Quite by accident, the researchers discovered that genetic inactivation of the p110g subunit leads to the development of invasive colorectal carcinomas in mice. In humans it has been previously found that p110g protein expression is lost in primary colorectal adenocarcinomas and in colon cancer cell lines. Overexpressing wildtype or kinase-dead p110g in human colon cancer cell lines with mutations of tumour suppressors, or with the oncogenes b-catenin and Ki-ras, suppressed tumorigenesis.

Penninger's group was examining genetically altered mice to determine how their white blood cells responded to infection when the mice lost weight, became sick and began to die. It turned out that they were riddled with colon cancer. Turning this discovery into practical medicine for the treatment of colon cancer in humans will obviously require time and a lot more study. However, it is hoped that this knowledge may help in the design of novel strategies for fighting colon cancer.

Colon cancers are the second leading cause of cancer death and it is estimated that 50% of humans develop colon tumours by the age of 70.

Source

1. Sasaki T, et al. Colorectal Carcinomas in Mice Lacking the Catalytic Subunit of PI(3)Kg Nature 2000 (406) 897-902.