News flashes are posted here frequently to keep you up-to-date with the latest advances in health and longevity. We have an unparalleled track record of breaking stories about life extension advances.
Long term chondroitin sulfate supplementation retards arthritis progression
Supplementing with chondroitin sulfate for two years reduces the progression of knee osteoarthritis according to the results of a recent clinical trial reported in the February issue of Arthritis & Rheumatism.
Andre Kahan of the University of Paris Descartes and his associates enrolled 622 osteoarthritis patients from France, Belgium, Switzerland, Austria and the United States for the current randomized, double-blinded trial. Three hundred nine participants received 800 milligrams chondroitins 4 and 6 sulfate, and 313 patients received a placebo daily for two years. Knee joint space width was measured by x-ray imaging of the affected knee at the beginning of the study and at 12, 18 and 24 months. Osteoarthritis symptoms and pain were also evaluated.
Participants who received chondroitin sulfate had significantly less joint space loss and less pain compared with those who received the placebo. The percentage of patients with joint space loss progression of at least 0.25 millimeters was 28 percent in the group that received chondroitin sulfate compared with 41 percent in the placebo group. Pain relief associated with chondroitin sulfate was evident during the first year of the study, and there were no differences in adverse events between the two groups.
The authors remark that the long-term structural effects observed in the current study may be due to the stimulation by chondroitin sulfate of anabolic activities in cartilage or depression of catabolic activities.
"The long-term combined structure modifying and symptom-modifying effects of chondroitin sulfate suggest that it could be a disease-modifying agent in patients with knee osteoarthritis," the authors conclude. "Further studies with longer follow-up and different outcome criteria are warranted to assess whether the beneficial structural changes associated with chondroitin sulfate demonstrated in our study are predictive of improvement in the long-term clinical progression of osteoarthritis."
Long life mutation in flies works by reducing free radicals
In an article published early online on January 21, 2009 in the Proceedings of the National Academy of Sciences, researchers from Brown University in Rhode Island, the University of Chicago, and the University of Connecticut Health Center report that a mutation that extends the lifespan of fruit flies works by limiting free radicals and the damage they cause. Free radicals are highly reactive cellular byproducts that damage tissue and contribute to many of the signs of aging.
Professor Stephen Helfand of Brown's Department of Molecular Biology, Cell Biology and Biochemistry and his associates sought to determine the life-extending mechanism of a mutation named "Indy" (which stands for "I'm not dead yet"), that he first discovered in 2000. Flies with the Indy mutation have double the average life span as those without it (70 versus 35 days). Dr Helfand's team compared gene expression in Indy flies and normal flies throughout their lives and determined that the mutation significantly limits the production of free radicals known as reactive oxygen species via reduced expression of genes involved in generating energy, without decreasing the overall level of energy (as assessed by measuring adenosine triphosphate levels) within the cell. Accordingly, protein carbonyls, a measure of free radical damage to proteins, were lower in the mitochondrial protein of Indy flies.
“There are very few, if any, interventions that are known to dramatically extend healthy lifespan,” Dr Helfand stated. “Understanding how … the Indy mutation alters the metabolic state of the fruit fly would allow someone to come up with pharmacological interventions that could mimic it and give you the benefit of genetic manipulation without having to do genetics.”
Greater vitamin K intake linked with reduced risk of advanced stage and high-risk prostate cancers
The January, 2009 issue of the journal Cancer Epidemiology, Biomarkers & Prevention published the finding of researchers at the German Cancer Research Center in Heidelberg of an association between a biomarker of vitamin K status and a lower risk of advanced stage and high-risk prostate cancers.
The study included participants in the EPIC-Heidelberg prospective cohort study who were free of cancer on enrollment. Vitamin K intake was estimated by evaluating responses to food frequency questionnaires, and by measuring serum undercarboxylated osteocalcin (ucOC), which is elevated when vitamin K intake is low, and intact total osteocalcin (iOC), which corresponds to total osteocalcin regardless of carboxylation status. Follow-up questionnaire responses obtained every 2 to 3 years over an 8 year period were used to ascertain prostate cancer diagnoses. The current study included 250 subjects who developed prostate cancer and 494 control participants.
When dietary intake of vitamin K was examined, men whose intake of vitamin K2 was in the top 25 percent of participants had a 64 percent lower risk of prostate cancer compared to men whose intake of the vitamin was in the lowest fourth. For every 10 micrograms per day increase in vitamin K2, an 11 percent reduction in the risk of prostate cancer was observed. Although the ratio of undercarboxylated osteocalcin to intact total osteocalcin was not found to be related to total prostate cancers, the researchers determined that a higher ucOC/iOC ratio (indicating a lower intake of vitamin K) predicted a greater risk of advanced stage and high risk disease.
“The increased risks of advanced-stage and high-grade prostate cancer with higher serum ucOC/iOC ratio strengthen the hypothesis that vitamin K status may play a role in the etiology and progression of prostate cancer,” the authors conclude.
Apples and Alzheimer's
The January 2009 issue of the Journal of Alzheimer's Disease reported the discovery of researchers at the University of Massachusetts of a protective effect of apple juice against the formation of amyloid-beta in the brains of mice. Amyloid-beta is a protein that forms plaques in the brain that characterize human Alzheimer's disease.
Amy Chan and Thomas B. Shea, PhD at the University of Massachusetts in Lowell sought to determine whether supplementation with apple juice could reduce the increase of amyloid-beta generation that has been shown to result from a deficiency of folate in mice deprived of the vitamin. For the current study, Drs Chan and Shea used normal mice and mice genetically altered to lack apolipoprotein E, a modification which causes the animals to exhibit greater oxidative stress in a manner similar to that of human Alzheimer's disease patients. The mice were given a diet supplemented with folic acid and vitamin E, or a diet deficient in these vitamins supplemented with iron, a pro-oxidant. Some of the animals on the deficient diet were provided with water that contained apple juice concentrate.
After one month, examination of the animals' brains revealed greater amyloid-beta levels in mice receiving the deficient diet compared with those who received the vitamin-supplemented diet. The addition of apple juice to the deficient diet significantly reduced amyloid-beta formation in both normal and genetically modified mice. The authors suggest that the mechanism of apple juice is partly attributable to its antioxidant potential, however, additional factors appear to be involved.
"These findings provide further evidence linking nutritional and genetic risk factors for age-related neurodegeneration and suggest that regular consumption of apple juice can not only help to keep one's mind functioning at its best, but may also be able to delay key aspects of Alzheimer's disease and augment therapeutic approaches," Dr Shea concluded.
B complex supplements reduce atherosclerosis progression in individuals with elevated homocysteine
An article published online on December 31, 2008 in the journal Stroke revealed the finding of the B-Vitamin Atherosclerosis Intervention Trial (BVAIT) of an inhibitory effect of high dose B vitamin supplementation on the progression of atherosclerosis among men and women with high homocysteine levels.
Howard N Hodis, MD, of the University of Southern California and colleagues assigned 506 men and postmenopausal women without cardiovascular disease who had an initial total homocysteine level of greater than 8.5 micromoles per liter to receive 5 milligrams folic acid, 50 milligrams vitamin B6 and 400 micrograms vitamin B12, or a placebo daily for an average of 3.1 years. Atherosclerosis was assessed via evaluation of carotid artery intima media thickness (CIMT), and fasting and post-methionine loading homocysteine levels were measured, upon enrollment and every six months.
Homocysteine levels decreased in subjects who received B vitamins, while an increase occurred in the placebo group. Post methionine loading homocysteine levels were found to be associated with carotid intima media thickness progression. When the entire group was considered, a reduction in the rate of the progression in carotid artery intima media thickness was associated with B vitamin supplementation, although the difference was not considered statistically significant. However, among participants whose homocysteine levels at the beginning of the study were at least 9.1 micromoles per liter, those in the placebo group had twice the rate of carotid artery intima media thickness progression than that observed among those who received B vitamins.
The authors suggest that the difference between the current trial's results and those of similar studies that did not find significant effects for B vitamins "may be the result of different timing of B vitamin supplementation according to the stage (early versus advanced) of atherosclerosis." They conclude that, "Further studies to determine whether reducing total homocysteine levels prevents plaque rupture and clinical events in a population similar to BVAIT are warranted."
Antioxidants relieve pancreatitis pain
A report published in the January, 2009 edition of the journal Gastroenterology revealed a pain relieving effect for antioxidants in men and women with chronic pancreatitis (CP). Pancreatitis, or inflammation of the pancreas, occurs with gallstones, alcohol abuse or genetic mutations, and the pain with onset can be sudden and severe. Chronic pancreatitis can lead to diabetes and impaired digestion.
Pramod Kumar Garg, MD, DM, of the All India Institute of Medical Sciences in New Delhi and his associates randomized 127 chronic pancreatitis patients to receive a daily placebo or the following antioxidants: 600 micrograms organic selenium, 540 milligrams ascorbic acid, 9000 international units (IU) beta-carotene, 270 IU alpha-tocopherol and 2 grams methionine. At the end of the six month treatment period, participants who received the placebo had twice the number of painful days and need double the number of analgesic tablets per month than those in the antioxidant group. While 13 percent of those who received the placebo reported becoming pain free, 32 percent of those in the antioxidant group experienced relief, with an effect noted as early as three months after beginning therapy.
"Abdominal pain, the predominant symptom in patients with chronic pancreatitis, is difficult to treat." stated Dr Garg. "The main reason for a largely ineffective medical treatment is that the mechanism of pain in CP is not well understood.
"Aside from medication, abstaining from alcohol and smoking are most important and key to halt the progression of CP," he added.
"We are encouraged by our findings, as significant improvement was noted with antioxidants in respect to all the parameters of pain in this study," Dr Garg concluded. "In addition, reduction in pain resulted in fewer man-days lost, thus providing functional employment gain to the patients. The findings should spur further research in this exciting area."