Life Extension Magazine September 2005
In The News
Intake of antioxidant-rich foods reduces brain damage from ischemic stroke and improves post-stroke movement recovery in test animals, according to scientists at the National Institute on Drug Abuse in Baltimore, MD.1
Previous studies have demonstrated that an antioxidant-rich diet protects aging animals from neurodegenerative changes. The Maryland study investigated a potential protective role of antioxidant-rich foods against ischemia, or lack of oxygen, as occurs with stroke.
For four weeks, adult rats were fed either a control diet or one supplemented with blueberry, spinach, or spirulina. Strokes were then surgically simulated in the rats. Those that received the blueberry-, spinach-, or spirulina-enriched diets had a significantly reduced volume of infarction in the cerebral cortex and an increase in post-stroke locomotor activity. Rats supplemented with blueberry or spinach had half as much brain damage as the control group, while the spirulina group had stroke lesions that were 75% smaller than those in the untreated group.1
Fruits and vegetables are rich sources of antioxidants, and abundant intake of these plant-based foods has been reported to help improve health and reduce the incidence of disease.2 Blueberries, spinach, and spirulina are rich in phytochemicals—including carotenoids, flavonoids, and anthocyanins—and have demonstrated particularly powerful antioxidant and free radical-scavenging activity.2,3 The Maryland study suggests a role for antioxidant-rich foods in protecting the brain against the effects of stroke.1
—Christie C. Yerby, ND
1. Wang Y, Chang CF, Chou J, et al. Dietary supplementation with blueberries, spinach, or spirulina reduces ischemic brain damage. Exp Neurol. May 2005;193(1):75-84.
2. Lako J, Trenerry C, Wahlqvist ML, Wattanapenpaiboon N, Sotheeswaran S, Premier R. Total antioxidant capacity and selected flavonols and carotenoids of some Australian and Fijian fruits and vegetables. Asia Pac J Clin Nutr. 2004;13(Suppl):S127.
3. Reddy MC, Subhashini J, Mahipal SV, et al. C-Phycocayanin, a selective cyclooxygenase inhibitor, induces apoptosis in lipopolysaccharide-stimulated RAW 264.7 macrophages. Biochem Biophys Res Commun. 2003 May 2;304(2):385-92.
Sigmoidoscopy fails to detect colon tumors in nearly two thirds of women who have them, according to a recent study published in the New England Journal of Medicine.* Sigmoidoscopy and colonoscopy are widely used screening tools to detect colon tumors. Both procedures use a long, flexible tube to inspect the colon for growths or polyps. The colonoscope is longer and is able to examine the entire six-foot length of the colon, while the sigmoidoscope examines only the lower two feet of the colon. Sigmoidoscopy is faster and less expensive than colonoscopy, and does not require the use of sedatives as colonoscopy does. However, the effectiveness of sigmoidoscopy is already in question, as studies in men have shown that it succeeds in detecting tumors in only 66% of average-risk men who have them.
The researchers studied nearly 1,500 women, aged 50-79, who were considered at average risk of colon cancer. Using colonoscopy, these asymptomatic women were screened for growths of the colon. The investigators then calculated how many women who had colon lesions would have been detected had sigmoidoscopy been used instead. Lesions were considered detectable by sigmoidoscopy if they were in the distal colon or if proximal colon tumors were accompanied by concurrent small adenomas in the distal colon, a finding that would have led to a colonoscopy.
Using colonoscopy as the primary screening tool, advanced neoplasia was found in 72 (4.9%) of 1,463 women. Had flexible sigmoidoscopy been used as the primary screening tool, advanced neoplasia would have been detected in only 25 (1.7%) of these women and missed in 47 (3.2%). Thus, only 35.2% of women with advanced neoplasia of the colon would have been identified using sigmoidoscopy alone. Colonoscopy thus appears to be more effective than sigmoidoscopy in screening women for colon cancer.
—Elizabeth Wagner, ND
* Schoenfeld P, Cash B. Flood A, et al. Colonoscopic screening of average-risk women for colorectal neoplasia. N Engl J Med. 2005 May 9;352(20):2061-8.
Emerging research suggests that the trace mineral selenium may be invaluable in the fight against prostate cancer.1 Selenium may help make prostate cancer cells more vulnerable to self-destruction, or apoptosis, report researchers at the Fox Chase Cancer Center in Philadelphia, PA.1
Selenium helps prostate cancer cells overcome their resistance to tumor necrosis factor-related apoptosis-inducing li-gand (TRAIL). An endogenously (internally) produced promoter of cell death, TRAIL is being researched as an experimental cancer drug. While TRAIL has shown promise against a wide variety of cancer cells, some cell types seem resistant to its effects.
Previous studies have demonstrated that selenium helps reduce prostate cancer risk, possibly by protecting prostate cells against DNA damage.2 The Philadelphia study took selenium research a step further, demonstrating that selenium sensitizes resistant prostate cancer cells to TRAIL, enabling the compound to destroy them.1 The researchers found that selenium contributed to an “amplification” loop in which the TRAIL drug set off a chain reaction of cell death among prostate cancer cells. Interestingly, neither selenium nor TRAIL was as effective on its own, indicating a synergistic effect of the two compounds.1
“The combination of a TRAIL and [selenium] may be a novel strategy for the development of innovative therapeutic modalities targeting apoptosis-resistant forms of prostate cancer,” concluded Vladimir M. Kolenko, MD, PhD, a lead author on the study.1
1. Yamaguchi K, Uzzo RG, Pimkina J, et al. Methylseleninic acid sensitizes prostate cancer cells to TRAIL-mediated apoptosis. Oncogene. 2005 May 16; [Epub ahead of print].
2. Waters DJ, Shen S, Glickman LT, et al. Prostate cancer risk and DNA damage: translational significance of selenium supplementation in a canine model. Carcinogenesis. 2005 Jul;26(7):1256-62.