What's Hot

What's Hot

March 2005

What's Hot Archive

March 30, 2005

Newly identified grape flavonoids can inhibit cancer growth

Researchers at the University of Illinois at Urbana-Champaign discovered that certain phytochemicals from the proanthocyanidin and anthocyanin classes of flavonoids found in grapes are effective at inhibiting an enzyme used by cancer cells to proliferate. Flavonoids include a number of water-soluble compounds responsible for the color in plants, whose health benefits are being increasingly revealed. The research was reported online on March 1 2005 in The Journal of Agricultural and Food Chemistry (http://pubs.acs.org/journals/jafcau).

University of Illinois professor in the department of natural resources and environmental sciences Mary Ann Lila, and colleagues analyzed the ability of grape cell cultures to inhibit human DNA topoisomerase II, an enzyme necessary for the growth of cancer. The researchers identified cyanidin-3,5-diglucoside, malvidin-3-acetylglucoside, peonidin-3-coumaryl-5-diglucoside, procyanidin B1, procyanidin B2, procyanidin B5, procyanidin dimer digallate, procyanidin C1, myricetin, and rutin, as having a synergistic benefit greater than resveratrol or quercetin, which have also shown anticancer effects. The compounds had less of an inhibitory effect on topoisomerase II when studied by themselves. Dr Lila commented, "We definitely had very potent activity against the particular antibody system we were using, which was that of the critical proliferation stage of carcinogenesis. In our subsequent studies now under way in animal models, we are getting direct evidence that these components in grapes work synergistically in fighting cancer. They have to work together to obtain the potency that works."

Elvira Gonzalez de Mejia, a professor in the department of food science and human nutrition who also worked on the project added,"Some of the compounds we identified have not been reported in cell culture and grapes. Some have high inhibitory activity in the promotion and progression stages of cancer and have a high probability to work against the disease."

—D Dye

March 28, 2005

Endothelial cells make C-reactive protein

In an article scheduled to appear in the April 2005 issue of American Journal of Pathology (http://ajp.amjpathol.org) researchers from the University of California Davis School of Medicine report that cells lining the arteries known as endothelial cells produce C-reactive protein, or CRP. CRP is a marker of inflammation that, when elevated in the blood, indicates increased heart disease risk, and is known to be made by the liver. The endothelial cells which line the arteries have been believed to offer protection against CRP. C-reactive protein induces endothelial cell dysfunction and plaque formation by causing the cells to produce less nitric oxide and by increasing cell adhesion molecules, allowing white blood cells to enter and damage the blood vessels.

Coauthor and professor of pathology and internal medicine at UC Davis Medical Center, Ishwarlal Jialal, explained their discovery: "This is an extremely important finding. We have convincingly demonstrated in this paper that aortic and coronary artery endothelial cells produce and secrete C-reactive protein. We also showed within the artery, mature white cells, called macrophages, make chemical messengers, cytokines, which enhance the C-reactive protein secretion by endothelial cells at least ten-fold."

He added, "This tells us that there is cross-talk in the active plaque where these cells act in concert to cause very high C-reactive protein levels in the atheroma, which is the accumulation of plaque on the innermost layer of the artery. The C-reactive protein produced by endothelial cells can not only act on the endothelial cells, but also on macrophages and smooth muscle cells in the atheroma. This creates a vicious cycle, leading to plaque instability and rupture, and ultimately heart attacks and strokes."

The authors also found that C-reactive protein causes endothelial cells to produce plasminogen activator inhibitor, which can lead to blood clot formation. Other research has indicated that plaque itself also makes CRP.

—D Dye

March 25, 2005

Aspirin may be useful to help prevent pre-eclampsia

Researchers led by Colin D. Funk of Queen’s University in Ontario, Canada have determined that low dose aspirin could be used to prevent and treat pre-eclampsia, a disorder that effects 5 to 10 percent of all pregnancies that can threaten both the mother and child. The disease is characterized by high blood pressure in the mother, and is believed to be linked with long-term heart disease in both the mother and child. The study was published online on March 17, 2005 in the Journal of Clinical Investigation.

Severe preeclampsia involves platelet activation, which aspirin blocks by inhibiting platelet PGH synthase-1 derived eicosanoids, however, their disruption delays the birth process. Dr Funk and researchers from the University of Pennsylvania, where Dr Funk was a previous faculty member, created a mouse model that mimics low dose aspirin therapy. They observed that the mice experienced normal labor induction, normal litter size and normal development of their young, with only slight alterations of ovarian and uterine environments.

Although administering aspirin to women at risk of pre-eclampsia is controversial due to possible problems with labor and blood clotting, Dr Funk, who was recently appointed as Canada Research Chair in Molecular, Cellular and Physiological Medicine concluded, “the rationale for low-dose aspirin therapy to prevent or delay pre-eclampsia without compromising reproductive function is definitely a feasible therapeutic strategy. This new mouse model will have significant value in studying the implications of low dose aspirin in several pathological conditions, such as pre-eclampsia, thrombosis, and inflammatory disorders. We’re hopeful that our model will lead the way to further treatment options for these debilitating conditions.”

—D Dye

March 18, 2005

Calcium supplements help build strong bones in teenaged boys

A study published on March 8 2005 online in Journal of Clinical Endocrinology & Metabolism found that boys who received calcium supplements had greater bone mineral content and were taller than those who did not receive the supplements. Improving bone mineral content early in life is believed to help reduce osteoporotic fractures later on.

Researchers at the Medical Research Council Human Nutrition Research, Elsie Widdowsom Laboratory in Cambridge, England, randomized 143 boys ages 16 to 18 to receive 500 milligrams calcium twice per day in the form of calcium carbonate, or a placebo for 13 months. Additionally, participants were grouped according to whether their activity level was high or low. Bone mineral content, bone area, lean and fat mass, height, and weight were measured before, during and following the treatment period.

Although both groups experienced increases in height, weight, lean and fat mass and most bone measurements over the course of the study, the group receiving calcium was found to have a significant increase in height, lean mass and bone mineral content of the whole body, lumbar spine and and hip compared to the boys who received a placebo. Adjustment for bone area and height lessened the increase in bone mineral content, which suggested that calcium's effect was accomplished through an effect on growth. Physical activity level appeared to increase the effect of calcium supplementation on bone mineral content only in an area of the upper leg bone.

The authors conclude that "calcium carbonate supplementation of adolescent boys increased skeletal growth, resulting in greater stature and bone mineral acquisition. Follow-up studies will determine whether this reflects a change in the tempo of growth or an effect on skeletal size that persists into adulthood."

—D Dye

March 16, 2005

Five percent reduction in calories provides significant reduction in cancer risk

A study  scheduled to be published in the May 2005 issue of the American Journal of Physiology-Endocrinology and Metabolism (http://ajpendo.physiology.org) found that reducing the calories of mice by only 5 percent was almost as effective as reducing calories by a third in preventing cell proliferation, an indicator of cancer risk.  Reducing the calories of laboratory animals by amounts as great as 50 percent in some studies has been found to reduce the risk of cell proliferation and cancer, as well as lengthen maximum lifespan.

Researchers at the University of California, Berkeley fed mice three days per week, which provided them with 5 percent fewer calories than those consumed by mice allowed to eat as much as they desired.  Other mice were fed diets containing 33 percent fewer calories than those consumed by the free fed mice. 

The researchers found that the three day per week regimen was nearly as effective as the more stringent 33 percent calorie restriction in reducing cell proliferation in breast, skin and T cells, compared to the free fed mice.  Lead investigator and professor of nutrition Marc Hellerstein, of the Department of Nutritional Sciences and Toxicology at UC Berkeley's College of Natural Resources explained, "Cell proliferation is really the key to the modern epidemic of cancer.  Normally, a cell will try to fix any damage that has occurred to its DNA.  But, if it divides before it has a chance to fix the damage, then that damage becomes memorialized as a mutation in the offspring cells. Slowing down the rate of cell proliferation essentially buys time for the cells to repair genetic damage."  

Lead author Elaine Hsieh observed, "Cutting just a few calories overall but feeding intermittently may be a more feasible eating pattern for some people to maintain."

—D Dye

March 14, 2005

AMA journal says vitamin E preventive benefit in macular degeneration outweighs possible risks

In an editorial published in the March 2005 issue of the American Medical Association journal Archives of Opthalmology (http://archopht.ama-assn.org) , Emily Y Chew, MD and Traci Clemons, PhD recommend that people at risk of macular degeneration continue to take 400 international units of vitamin E per day, despite the questionable and widely publicized results of a vitamin E meta-analysis published earlier this year that concluded an increased mortality risk for "high-dose" users of the vitamin. The 400 iu dosage of vitamin E is part of a supplement formulation tested in the Age-Related Eye Disease Study (AREDS), which involved men and women at risk of advanced macular degeneration. The formula, which also contained 15 milligrams beta-carotene, 500 milligrams vitamin C, 80 milligrams zinc oxide and 2 milligrams copper, was determined to be protective against the progression of the disease.

AREDS found a 25 percent reduction in the risk of developing advanced age-related macular degeneration and a 19 percent lower risk of moderate vision loss among participants who received the supplement formula compared to the placebo group. Individuals taking the AREDS formula actually had a mortality risk that was 14 percent lower after an average of 6.5 years of supplementation compared to those who received the placebo. In the meta-analysis of vitamin E and mortality, of the three studies involving 400 international units per day, which is a commonly consumed dose, participants who received vitamin E were slightly more likely to be living after 5 years than those who received the placebo.

Concerning the vitamin E meta-analysis, which appeared in the Annals of Internal Medicine, the authors comment that the inclusion of 400 IU in the "high dose" group seemed "somewhat arbitrary." They also noted that the statistic model used was dependent upon assumptions concerning dose-response behavior that may not be correct. They recommend that that those at risk of advanced macular degeneration continue to take the AREDS formula.

—D Dye

March 11, 2005

Blood marker predicts heart disease mortality

Blood levels of a peptide hormone can help predict mortality risk in patients with known but stable coronary artery disease, as reported by Danish researchers.*

Following its release, the hormone is split into two byproducts: brain natriuretic peptide (BNP) and its fragment, NT-pro-BNP. BNP is useful in rapid, accurate diagnosis of heart failure, while both BNP and NT-pro-BNP can reliably predict mortality in patients with acute coronary syndromes. NT-pro-BNP levels are known to rise after a heart attack.

The Danish study followed 1,034 patients with signs or symptoms of coronary artery disease who were referred for angiography. Blood NT-pro-BNP levels were elevated in all subjects compared to those without coronary artery disease. After nine years of follow-up, subjects with the highest NT-pro-BNP levels had a significantly higher rate of mortality than those with the lowest levels. Higher levels of NT-pro-BNP were correlated with more serious coronary artery disease, lower left ventricular ejection fraction, and a decreased marker of kidney function.

After adjusting for other risk factors, NT-pro-BNP level was found to be an independent predictor of survival in patients with stable coronary artery disease. Because NT-pro-BNP is elevated by each ischemic event, its correlation with greater mortality may reflect the frequency of such coronary events.

For the first time, patients with known coronary artery disease can be monitored using simple laboratory testing rather than invasive procedures. These findings also suggest that NT-pro-BNP may be suitable as a screening tool for undiagnosed coronary artery disease.

—Linda M. Smith, RN

*Kragelund C, Gronning B, Kober L, Hildebrandt P, Steffensen R. N-terminal pro-B-type natriuretic peptide and longterm mortality in stable coronary heart disease. N Engl J Med. 2005 Feb 17;352(7):666-75.

March 9, 2005

Aspirin lowers women's stroke risk

An early release published online on March 7 2005 in the New England Journal of Medicine (www.nejm.org) reported conclusions from The Women's Health Study that low dose aspirin reduced the risk of stroke in older women. The Women's Health Study was a ten year randomized double-blind trial that investigated the effect of aspirin on cardiovascular disease on 39,876 healthy women over the age of 45. Previous studies have found that aspirin reduces the risk of a first heart attack in men.

Half of the women in the trial received 100 milligrams aspirin every other day, while the remainder received a placebo. During the follow-up period, 477 cardiovascular events occurred among the women who received aspirin compared to 522 in the placebo group. This 9 percent reduction in risk was not considered signficant by the researchers, however, when women aged 65 and older were analyzed separately they were found to have experienced a 26 percent reduction in cardiovascular events. When stroke was analyzed, a signficant difference between the aspirin and placebo groups emerged, with a 17 percent lower risk of stroke experienced by women who received aspirin. Women over 65 again had greater benefits, with a 30 percent reduction in ischemic stroke risk associated with aspirin. The benefit of aspirin was consistent throughout the trial, refuting the concern that aspirin's ability to inhibit platelet function diminishes with time.

The authors of the report state that the Women's Health Study's results are particularly relevant since women have a relatively greater proportion of strokes than of heart attacks compared to men. They note that they cannot rule out the possibility that the lack of a significant reduction in heart attack in this study could be due to an insufficient dose of aspirin, or to taking the drug on alternate days.

—D Dye

March 7, 2005

Inflammation in rheumatoid arthritis linked to cardiovascular disease mortality

The March 2005 issue of Arthritis & Rheumatism (http://www.rheumatology.org/publications/ar) published the findings of Mayo Clinic epidemiologists that the body-wide inflammation of rheumatoid arthritis may be to blame for the increased risk of cardiovascular death in patients with the disease. Individuals with the disease have been shown to have a greater risk of dying of cardiovascular disease if they have large joint swelling, inflammation of the blood vessels (vasculitis), rheumatoid lung disease or a high erythrocyte sedimentation rate (ESR), which measures inflammation in the body.

Hilal Maradit Kremers, MD, and colleagues followed 603 Rochester, Minnesota residents diagnosed with rheumatoid arthritis between 1955 and 1995. Information on cardiac events, cardiovascular risk factors, indicators of systemic inflammation, and information concerning rheumatoid arthritis severity was collected, as well as data on the presence of additional diseases. The subjects were followed until death or January of 2001.

Three hundred fifty-four patients died during follow up, for which cardiovascular disease was the cause of death for 176. The risk of dying from cardiovascular disease was significantly higher among subjects who had experienced at least three elevations of ESR values, inflammation of the blood vessels, and rheumatoid lung disease, with the presence of any of these factors more than doubling cardiovascular mortality risk.

Although the precise mechanism by which the inflammation of rheumatoid arthritis causes heart disease is not known, the researchers believe that if the process is kept under control, cardiovascular mortality could be lowered.

Senior author and Mayo Clinic rheumatologist and epidemiologist, Sherine Gabriel, MD, commented, "Our previous research showed that rheumatoid arthritis patients have a higher risk of early death than others and that these deaths are mostly due to cardiovascular disease. We suspect that systemic inflammation promotes this risk. Our findings support this hypothesis."

—D Dye

March 4, 2005

Higher vitamin E levels mean lower prostate cancer risk

In a Brief Communication published in the March 2 2005 issue of the Journal of the National Cancer Institute, researchers from the National Cancer Institute and the National Public Health Institute in Helsinki, Finland found a correlation bewtween high serum tocopherols and a lower risk of developing prostate cancer. Alpha and gamma-tocopherol are two forms of vitamin E, alpha-tocopherol being the form most found in blood plasma and gamma-tocopherol being the form that occurs most in foods.

The National Cancer Institute's Demetrius Albanes, MD, and colleagues analyzed data from the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, which found an association between supplementation with vitamin E and lower risk of prostate cancer among 29,1333 men. For the current study, the researchers selected 100 participants who had developed prostate cancer during the ATBC study follow-up, and matched them with 200 subjects who did not have the disease. Blood samples analyzed upon enrollment provided information on serum alpha and gamma-tocopherol concentrations.

The team discovered that men who had the highest concentrations of alpha and gamma-tocopherol at the beginning of the study experienced a reduced risk of prostate cancer compared to men with the lowest circulating levels. Men whose levels of alpha-tocopherol with in the top one-third of participants had a 51 percent lower risk of developing prostate cancer than those whose levels were in the lowest third. Gamma-tocopherol appeared to be similarly protective, with a 43 percent lower risk experienced by those whose levels were in the top third compared to the lowest third.

The authors remarked that "the findings of this study were accentuated among men who received alpha-tocopherol supplementation, which may allay concerns regarding whether supplementation with alpha-tocopherol may negatively impact gamma-tocopherol status in other prevention trials such as the Selenium and Vitamin E Cancer Prevention Trial."

—D Dye

March 2, 2005

Folic acid and B12 reduce post-stroke fracture risk

The results of a study published in the March 2 2005 issue of the Journal of the American Medical Association revealed that supplementation with folic acid and vitamin B12 after a stroke reduces the risk of hip fracture. Stroke patients have up to four time the risk of incurring a fracture than healthy individuals, possibly due to an increase in levels of homocysteine, an amino acid which, when elevated, is associated with increased cardiovascular disease including stroke, as well as a greater risk of osteoporosis. The vitamins folic acid and B12, as well as other nutrients, are known to help decrease serum homocysteine levels.

Yoshihiro Sato, MD, of Mitate Hospital in Tagawa, Japan, and colleagues recruited 628 men and women who had hemiplegia resulting from a stroke that occurred within the previous year. Three hundred fourteen patients were administered 5 milligrams folic acid and 1500 micrograms vitamin B12 per day, and an equal number received a placebo for two years. Participants were asked to record any falls that occurred. Five hundred fifty-nine patients completed the study.

At the study's conclusion, 27 hip fractures had occurred in the placebo group, compared to 6 that had occurred amongst those who received folic acid and vitamin B12. When total fractures were compared, 32 placebo patients and 8 who had received the vitamins experienced fractures of any type. Homocysteine levels increased by 31 percent in the group who received the placebo, while declining by 38 percent in the vitamin-treated group.

In an accompanying editorial, Joyce B.J. van Meurs, PhD, and André G. Uitterlinden, PhD, from the Erasmus Medical Center, in Rotterdam, the Netherlands, write, "After the initial observation of association between circulating homocysteine levels and fracture risk less than one year ago, these results now support a causal link."

—D Dye

March 1, 2005

Prostate drug could save lives

A study published in th April 1 2005 issue of the American Cancer Society journal Cancer found that the drug finasteride, marketed as Proscar, could save lives by preventing prostate cancer. Earlier findings from the Prostate Cancer Prevention Trial (PCPT)had determined that the use of finasteride offered protection from the disease but a possible increase in high grade tumors in those who did develop prostate cancer prompted the need for further analysis in regard to a decline in mortality among those taking the drug.

Finasteride is commonly prescribed to men as a treatment for benign prostate enlargement and male pattern baldness. The drug works by inhibiting the enzyme 5-alpha-reductase, thereby helping to prevent the production of dihydrotestosterone, a hormone that stimulates growth of the prostate. Another compound used to treat enlargement of the prostate, saw palmetto extract, is believed to inhibit 5-alpha-reductase in the prostate gland, but not in the blood.

For the current analysis, Joseph M. Unger, MS and colleagues from the Southwest Oncology Group Statistical Center at the Fred Hutchinson Cancer Research Center in Seattle applied epidemiologic data to the Prostate Cancer Prevention Trial results. The trial found a 24.8 percent reduction in new cases of prostate cancer in men taking finasteride compared to those who received a placebo over a seven year period, which the researchers determined would save 316.760 person-years over a ten year period. Although an increase of 6.9 percent in the proporton of high grade tumors occurred in users of finasteride, lives saved by the drug would still amount to 262,567 person years.

The authors conclude, "even if finasteride is found to potentiate the growth of high-grade tumors, this analysis shows that the potential detrimental effects of an increased rate of cases with high grade Gleason score would be substantially outweighed by a reduction in incidence."

—D Dye

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