Diet and Exercise Are Key Factors in Determining Lung Cancer Risk

http://www.medscape.com/viewarticle/567225

December 10, 2007 (Philadelphia, Pennsylvania) — Smoking is not the only factor to be considered in the determination of a person's risk of developing lung cancer, according to a recent study presented at the American Association for Cancer Research (AACR) 6th Annual International Conference on Frontiers in Cancer Prevention Research. This study, highlighted at an AACR press conference on the effects of lifestyle on cancer prevention, suggested that, in addition to smoking, diet and physical activity are key in determining a person's overall risk of developing lung cancer. This is important, especially when considering that although smoking is the leading cause of lung cancer, approximately 15% of all lung cancers are diagnosed in people who have never smoked.
"The way we live our lives does influence our risk of getting cancer," said Tim Byers, MD, professor of preventative medicine at the University of Colorado, in Aurora, who was not involved in the study. "Choices we make in tobacco use, sun exposure, food, and physical activity all seem to add up to explain half or more of cancer risk in the population."
Recently, a model to predict lung cancer development in never, former, and current smokers was developed. Although this Spitz model showed clear associations with lung cancer development and smoking history, family history of respiratory disease, and exposure to second-hand smoke or dust, the model did not take into account the relative contributions of several other factors. In the current study, presented by Michele Forman, PhD, from the University of Texas MD Anderson Cancer Center, in Houston, fruit and vegetable intake, as well as physical activity, were examined as potential risk factors. According to Dr. Forman, this study was the first risk-prediction model for lung cancer that took into account, in addition to smoking, both diet and physical activity.
Data were obtained from the same people used in the generation of the Spitz model. Participants included lung cancer patients enrolled from the University of Texas MD Anderson Cancer Center and healthy matched controls recruited from a local private-physician clinic group. The controls were matched on age, sex, and smoking status. All study participants were categorized as either never, former, or current smokers.

Vitamin C in the Management of Erythropoetin-resistant Anemia in Chronic Kidney Disease

A role for vitamin C in erythropoetin-hyporesponsive patients has been suggested, despite the lack of evidence to suggest a mechanism of action. A possible mechanism could be related to the antioxidant properties of vitamin C and to its effects on iron metabolism or endogenous erythropoetin synthesis.
The efficacy of vitamin D has been evaluated in clinical trials. A prospective, randomized, crossover study evaluated 27 hemodialysis patients with functional iron deficiency.[1] All patients who were administered 500 mg of intravenous vitamin C 3 times weekly for 3 months had significant increases in hemoglobin and transferrin saturation, and hemoglobin and transferrin saturation declined after cessation of vitamin C therapy. Sezer and colleagues[2] also reported a significant increase in hemoglobin concentration and a decrease in the dose of recombinant human erythropoetin (EPO) in 36 hemodialysis patients whose ferritin level was > 500 g/L after 8 weeks of treatment with vitamin C at a dosage of 1 g/wk.
More recently, this has been tested in a prospective, randomized, crossover study.[3] Approximately 65% of hemodialysis patients responded to treatment with 1500 mg/wk of intravenous vitamin C over a 6-month period with almost a 2 g/dL increase in hemoglobin concentration, together with a 2500 IU/wk (30%) reduction in EPO dose. Nevertheless, the K/DOQI Work Group for guideline 3.3.1 L stated: "in the opinion of the Work Group, there is insufficient evidence to recommend the use of vitamin C (ascorbate) in the management of anemia in patients with CKD." Furthermore, long-term high doses of vitamin C treatment might be a potential risk for the development of secondary oxalosis in patients with end-stage renal disease.