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What's Hot

February 2003

What's Hot Archive

February 28, 2003

Vitamin D supplements prevent fractures in older men and women

The British Medical Journal's March 1 2003 issue published the results of a trial by UK researchers showing that vitamin D supplements prevent fractures without any adverse effects.

The researchers recruited 2,037 men and 649 women ages 65 to 85 who were not already taking vitamin D supplements and who were free of conditions that were contraindications for vitamin D supplementation. Participants were sent a capsule containing 100,000 international units vitamin D3 (also known as cholecalciferol) or a placebo every four months for five years, along with a questionnaire that asked participants whether a major illness or bone fracture had occurred. A subgroup of subjects received serum analysis of vitamin D and parathyroid hormone levels after four years.

At the study's conclusion, 268 fractures had been reported. One hundred forty-seven of the fractures were of the hip, wrist, forearm or vertebrae, fracture sites commonly seen with osteoporosis. The group receiving vitamin D was found to have a 22% lower incidence of a first fracture at any site and one third lower rate of a fracture occurring in the hip, wrist, forearm or vertebra. Serum parathyroid hormone concentrations were only slightly lower in the group receiving the vitamin than the control group.

During the trial, the deaths of 471 participants were ascertained. Interestingly, the vitamin D group experienced a risk of dying from all causes that was 12% lower than those who received the placebo.

The authors mention that previous studies using lower doses of vitamin D may not have provided high enough levels of the vitamin to achieve a significant effect. The current study, which provided an equivalent to over 800 international units per day for a significant length of time, provided a dose high enough to provide benefits without side effects, and at minimal cost.

—D Dye


February 26, 2003

Mixed tocopherols better at preventing platelet aggregation

A study published in the March 2003 issue of the American Journal of Clinical Nutrition showed a mixture of tocopherols, rich in the gamma-tocopherol fraction of the vitamin, to be more effective than alpha-tocopherol in inhibiting platelet aggregation. Prevention of blood clots through platelet aggregation inhibition has long been attributed to vitamin E, and alpha-tocopherol has until recently been the only form of the vitamin to be recognized.

Researchers at the University of Uppsala in Sweden randomly provided forty-six participants with an alpha-tocopherol supplement, mixed tocopherols or a placebo for eight weeks. Blood samples were taken at the study's onset and at the end of the eight week period. The samples were tested for platelet aggregation in response to two different inducers, nitric oxide release, activation of endothelial constitutive nitric-oxide synthase and protein kinase C, and platelet content of superoxide dismutase and other factors.

Platelet aggregation was significantly reduced in the group receiving mixed tocopherols, but not in the groups receiving alpha-tocopherol or the placebo. Nitric oxide release and endothelial constitutive nitric-oxide activation were increased in the groups receiving tocopherols, but more so in the mixed tocopherols group. Platelet superoxide dismutase was also increased in the tocopherol groups, while protein kinase C activation was decreased.

Although epidemiologic studies have demonstrated a lower cardiovascular event risk associated with a higher intake of vitamin E from diet, studies administering the vitamin as a supplement have provided conflicting results. The fact that alpha-tocopherol was the only vitamin E fraction used in these studies, and the evidence obtained in this study of a greater benefit from mixed tocopherols on platelet aggregation and factors involved with platelet aggregation may be an explanation for this puzzling dichotomy.

—D Dye


February 24, 2003

Zinc, beta-cryptoxanthin may protect against rheumatoid arthritis

The February 15 issue of American Journal of Epidemiology published the results of a study that determined the effect of the intake of various antioxidants on the risk of developing rheumatoid arthritis. Lead author James R Cerhan of the Mayo Clinic and colleagues analyzed data provided by 29,368 participants who enrolled in the Iowa Women's Health Study in 1986. The women completed questionnaires at the study's onset which provided data on the frequency of consumption of 127 foods as well as on the use of nutritional supplements. The participants also reported information on medical history, smoking history, and other lifestyle factors. Follow-up surveys were mailed in 1987, 1989, 1992 and 1997 to update information. The last two surveys asked the participants if they had ever been diagnosed with rheumatoid arthritis, and if so, at what age. Respondents whose rheumatoid arthritis was diagnosed before 1987 and cases that could not be validated were excluded from the analysis, leaving 152 cases of the disease to be analyzed.

The researchers found a reduction in the risk of rheumatoid arthritis associated with consumption of zinc supplements. This was not seen when zinc from both food and supplements combined was studied. The carotenoid beta-crypotoxanthin also showed an inverse association with rheumatoid arthritis risk. Consumption of fruits and cruciferous vegetables were inversely associated with disease incidence, although less strongly.

The authors note that zinc is essential for normal immunologic function and is an inducer of metallothionine, which acquires zinc or copper as a cofactor and functions as an oxygen radical scavenger. Zinc is also cofactor for superoxide dismutase, which detoxifies superoxide radicals. Beta-cryptoxanthin as well is an antioxidant. If the findings of the researchers can be confirmed, they would provide one of the few modifiable protective factors for rheumatoid arthritis.

—D Dye


February 21, 2003

Deprenyl helps smokers quit

In the January 15, 2003 issue of the journal Biological Psychiatry, researchers led by Dr Tony George of Yale University's Transdisciplinary Tobacco Use Research Center found that selegiline hydrochloride, also known as deprenyl, was beneficial in enabling smokers to quit. In a study funded by the NIDA, forty smokers received selegiline hydrochloride or a placebo daily for one week and twice daily for seven weeks. Prior to the study, and after each month, the subjects received tests that assessed nicotine dependence and nicotine craving intensity. Individuals with severe depression were excluded from the trial.

On the fifteenth day of the study on which the subjects were scheduled to attempt to give up smoking they received smoking cessation counseling, which included relapse prevention strategies and motivational enhancement. Participants' breath and plasma were regularly analyzed to verify their abstinence. The drug and placebo treatments were tapered off before discontinuation at the study's conclusion. Participants were followed up at six months to determine their abstinence rates.

During the study's final month, 30 percent of selegiline-treated patients reported complete abstinence compared to 5 percent in the placebo group. At two months, 45 percent of those who received selegiline had quit smoking and compared to a rate of 15 percent in those not receiving the drug . After six months, 20 percent of the selegiline group were still not smoking while only 5 percent of the placebo users remained free of the habit.

Selegiline hydrochloride is a monoamine-oxidase B inhibitor that helps prevent the breakdown of dopamine. Because a reduction in dopamine levels has been associated with the symptoms of nicotine withdrawal, preventing the breakdown of dopamine with this drug may help people quit smoking.

—D Dye


February 19, 2003

Vitamin B1 derivative prevents diabetic complications

An advance online publication in the journal Nature Medicine reported a treatment that blocked three of the four pathways of blood vessel damage in diabetes in laboratory experiments. The drug, benfotiamine, is a synthetic derivative of thiamine, also known as vitamin B1. Blood vessel injury in diabetics is the leading cause of blindness, kidney failure, heart disease and leg amputation that occurs in this population. Benfotiamine has been prescribed in Europe to treat diabetic neuropathy and sciatica for three decades but has never been clinically tested.

In diabetic patients, cells are nourished by blood that is high in glucose, but most can keep their internal glucose at a normal level. However, some cells, in particular the endothelial cells lining the arteries and the capillaries of the kidney and retina, cannot manage glucose and develop high internal levels This causes glucose-derived intermediate metabolic products to accumulate inside the cell which activates pathways of cellular damage that leads to the devastating conditions associated with diabetes. Two of these intermediates are the end products of another pathway mediated by the enzyme transketolase. The researchers hypothesized that boosting the activity of the enzyme might reverse the pathway and convert the two harmful intermediates into harmless substances, thereby preventing the activation of three of the damaging pathways.

While vitamin B1, a cofactor for transketolase activity, increased the enzyme's activity by 20%, the fat-soluble thiamine derivative benfotiamine boosted it by 300 to 400 percent, and when tested in endothelial arterial cells it was found to block all three destructive pathways. When given to rats, the drug prevented diabetic retinopathy. Senior researcher Dr Michael Brownlee of the Albert Einstein College of Medicine stated, "Benfotiamine has been used extensively in Germany for many years, and to my knowledge there are no reported side effects."

American Stroke Association spokesperson, Robert J. Adams, MD, added, "There is currently great interest in studying herbs used in traditional forms of medicines, and the problem of dementia after stroke is a significant one. As the authors point out, this work showing that ginseng may improve memory after stroke needs to be further studied, with larger sample sizes. A placebo-controlled study would also be the next step."

—D Dye


February 17, 2003

Ginseng improves memory after stroke

The 28th International American Stroke Association's Stroke conference was the site of a presentation by Chinese researchers who reported that ginseng improved the memory of individuals afflicted with dementia following a stroke. Ginseng has previously been found to increase the activities of the brain chemicals acetylcholine and choline acetyltransferase in older mice.

Forty patients who had mild to moderate vascular dementia resulting from small strokes participated in the study. The researchers gave 25 patients an extract from Chinese ginseng roots three times daily, while the remainder of the patients received the drug Duxil, which is a combination of the drugs almitrine and raubasine, used to oxygenate brain tissue to improve memory in dementia patients. Prior to the study and at its conclusion at twelve weeks, the subjects were given tests which assessed immediate and delayed story recall, delayed word recall, verbal learning, visual recognition and verbal recognition. Ginseng was found to significantly improve average memory function at the end of the study.

Lead researcher Jinzhou Tian, M.D, of Beijing University of Chinese Medicine, in Beijing, China, commented, "Chinese ginseng has been used for centuries in China to treat disease and aging . . . . However, the effects of Chinese ginseng compound on mild and moderate dementia after stroke in humans have not been reported until now."

American Stroke Association spokesperson, Robert J. Adams, MD, added, "There is currently great interest in studying herbs used in traditional forms of medicines, and the problem of dementia after stroke is a significant one. As the authors point out, this work showing that ginseng may improve memory after stroke needs to be further studied, with larger sample sizes. A placebo-controlled study would also be the next step."

—D Dye


February 14, 2003

Calorie restriction delays onset of Huntington's disease symptoms in mice

The Proceedings of the National Academy of Sciences Online Early Edition published evidence this week that reducing calorie intake delays the beginning of Huntington's disease symptoms and prolongs the lifespan of mice genetically modified to develop the disease. Huntington's disease is an inherited condition that causes the degeneration of neurons in specific areas of the brain, resulting in uncontrolled movements, loss of intellectual faculties, and emotional problems.

The National Institute on Aging researchers inserted the abnormal gene that causes the disease into a group of mice and found that the animals showed all of the signs of Huntington's, including an altered metabolism resembling diabetes which caused weight loss. Their brains showed neuron degeneration of the region that helps cont rol body movements that degenerates in human Huntington's disease.

NIA Laboratory of Neurosciences chief, Mark Mattson, PhD, previously discovered that maintaining rats on low calorie diets or feeding them every other day improved glucose metabolism and protected brain cells in models of stroke and Parkinson's disease. In the current study, mice with the Huntington's disease gene who were maintained on an every other day regimen of feeding during adulthood developed the disease an average of twelve days later and lived 15 percent longer than mice allowed to consume as many calories as they wanted. They also had better regulation of glucose, did not lose weight as quickly, and examination of their brains showed less neurodegeneration and higher levels of heat shock protein and brain-derived neurotrophic factor, which increase cellular resistance to stress and stimulate the growth of nerve cells, respectively. Dr Mattson explained, "If reducing food intake has the same effects in humans as it does in mice, then it may be theoretically possible to delay the onset of the disease and extend the lives of Huntington's patients by prescribing low-caloric diets or diets with reduced meal frequency."

—D Dye


February 12, 2003

Calcium's mechanism in slowing colorectal cancer growth discovered

It has been known for years that calcium plays a role in the prevention of colon polyps and cancer. A report published in the February 10 2003 online edition of the Proceedings of the National Academy of Sciences revealed that a bacterial toxin that causes traveler's diarrhea previously shown to slow colon cancer growth opens a cellular door to allow calcium into tumor cells. This slows the growth of the tumor cells, although it does not destroy them.

Researchers at Thomas Jefferson University in Philadelphia had found that the toxin interfaces with a receptor known as GCC on the cell surface of metastatic colon cancer cells. This slows their growth and spread by lengthening the time of cell cycle growth. In the current study, the researchers discovered how this occurs.

Assistant professor of medicine at Jefferson Medical College of Thomas Jefferson University, GianMario Pitari, MD, PhD, explained, "Dietary calcium is the mediator of this antiproliferative effect. Now, we show that one of the mechanisms by which dietary calcium works is through this pathway. The toxin activates the receptor, GCC, causing an opening of a channel and an influx of calcium into the tumor cell. This influx causes a reduction of cancer cell growth. Somehow there is an interaction between the toxin and dietary calcium in blocking the growth of the tumor. The mechanism by which this occurs is very specific and a completely new pathway. No one has linked this pathway to antiproliferation and inhibition of tumor DNA synthesis . . . We think you can use the toxin as an intravenous infusion to treat cancer metastases. The toxin will not cross the intestinal lumen, meaning there won't be the side effects of diarrhea."

—D Dye


February 10, 2003

Omega-3 fatty acids enhance plaque stability

The February 8 2003 issue of the journal The Lancet published the results of a clinical trial of omega-6 fatty and omega-3 fatty acids which found that omega-3 fatty acids helped enhance the stability of atherosclerotic plaques. Unstable plaques are more vulnerable to rupture, leading to thrombosis-mediated cardiovascular events. In this study, atherosclerotic plaques incorporated omega-3 fatty acids into their structure, which caused changes that improved their stability.

Researchers at the University of Southampton, Southampton England, randomized 162 patients scheduled for carotid endarterectomy (surgical removal of the inner layer of the artery) to receive six capsules containing fish oil that provided 1.4 grams omega-3 fatty acids, sunflower oil that provided 3.6 grams of the omega-6 fatty acid linoleic acid, or an oil blend designed to provide the intake of the average adult diet as a control. Participants were advised to consume the capsules daily until their surgeries.

When the arterial plaques were examined following the surgery, the researchers found that the proportions of omega-3 fatty acids EPA and DHA were higher in the group receiving fish oil than the controls. Sunflower oil was found to have little effect on the fatty acid composition of plaques. More plaques from patients who received fish oil had thick fibrous caps and less signs of inflammation compared to the other groups, indicating greater stability. The fish oil group also had lower triglycerides after treatment than the other two groups.

A reduction in fatal and nonfatal cardiovascular events has been associated with increased consumption of omega-3 fatty acids from fish oil. The enhancement of plaque stability provided by omega-3's could provide an explanation for this observation. The findings of the present study support the hypothesis that "atherosclerotic plaques are dynamic and responsive to dietary modification, which can affect plaque stability." (Thies F et al, "Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomized controlled trial", Lancet 2003; 361:477-85.)

—D Dye


February 7, 2003

JAMA study recommends acetylcysteine to prevent contrast nephrotoxicity in patients with kidney impairment

The use of contrast media in coronary angiography is considered safe for most individuals, however, patients challenged with kidney dysfunction, diabetes mellitus and congestive heart failure are at risk of acute contrast nephropathy, which is a deterioration of kidney function that can result in long term renal impairment and has been associated with increased length of hospital stays and greater mortality. The amino acid acetylcysteine is an antioxidant that has been shown to prevent the condition in individuals with impaired kidney function who undergo CT scans. To determine the effect of acetylcysteine in coronary angiography, researchers in Hong Kong studied 200 Chinese patients with moderate renal insufficiency who were scheduled for the procedure.

The subjects were randomly administered 600 milligrams oral acetylcysteine or a placebo twice per day on the day of the procedure and the previous day. Both groups received a low-osmolarity contrast agent.

Four patients who received acetylcysteine compared with twelve patients in the placebo group experienced an increase of greater than 25% in serum creatinine within the two days following coronary angiography. Because the kidneys filter creatinine and other substances from the blood, creatinine elevation indicates a decline in kidney function. Within the 48 hour period following angiography, serum creatinine on average was lower in the acetylcysteine group, and following this period, creatinine clearance was increased.

The study was published in the February 2003 issue of the Journal of the American Medical Association. In an accompanying editorial, Gary C Curhan MD wrote, "The reduction in length of hospitalization alone... is sufficient to recommend considering this approach for patients with reduced renal function who will undergo any procedure in which an intravenous or intra-arterial iodinated contrast agent will be administered."

—D Dye


February 5, 2003

Tea and soy synergistically help to prevent prostate cancer in mice

In a study published in the February 2003 issue of the Journal of Nutrition, researchers from Harvard Medical School found that a combination of green tea and soy or black tea and soy resulted in the prevention of prostate tumor cell growth and metastasis in mice. Asian men, who consume high amounts of tea and soy, have a significantly lower incidence of prostate cancer.

Ninety-six eight week old male mice were divided into six groups who received one of the following regimens added to their diets for a two week period: soy protein concentrate, black tea infusion, green tea infusion, soy protein concentrate and black tea infusion, soy protein concentrate and green tea infusion or an unenhanced control diet. The animals were then inoculated with a human prostate cancer cell line and toninued on their dietary regimen. Ten weeks following tumor cell inoculation the mice were examined for tumors.

All three supplements were found to reduce the formation and proliferation of tumors compared to the mice who received the control diet. The soy protein and black tea regimens also reduced final tumor weight. The combination of black tea and soy protein was found to be synergistic in the prevention of new tumor formation, and metastases to lymph nodes, and in reducing final tumor weight. Green tea combined with soy protein also showed a synergistic effect in reducing tumor weight and metastasis and reduced testosterone and dihydrotestosterone (DHT), hormones believed to fuel prostate cancer growth. Green tea given alone, however, was associated with an increase in serum testosterone and DHT.

The study is the first, to the authors' knowledge, to demonstrate the synergy of two major components of the Asian diet in protecting against prostate cancer.

—D Dye


February 3, 2003

Antioxidant vitamins help insulin treat diabetes

A study conducted at the University of California Irvine College of Medicine revealed that the antioxidant vitamins C and E, when combined with insulin therapy in diabetic rats, enhanced insulin's blood sugar-lowering effect and helped protect the animals' organs from damage. While insulin successfully treats elevated blood sugar, complications such as heart disease and nerve, liver and kidney damage are seen in many diabetic patients. The report was published in the January 2003 issue of the journal Kidney International.

The researchers, led by professor of medicine Dr Nick Vaziri, found that diabetes, left untreated, resulted in hypertension and increased free radical production, which converted sugars and proteins into harmful compounds, leading to tissue damage. When rats in whom diabetes was induced were treated with insulin alone, blood pressure was lowered to a degree and the free radical attack on sugars and proteins lessened, however free radical attack on nitric oxide was significantly increased. Nitric oxide is found throughout the body and offers protection against free radicals. When the compound is subjected to free radical attack, it results in even greater damage.

When vitamins C and E were administered with insulin, blood sugar was lowered, and sugars and proteins as well as nitric oxide were protected from free radical attack. Dr Vaziri explained, "Blood pressure was lowered to normal, and free radicals were not in sufficient numbers to degrade the sugars, proteins and nitric oxide. We think this shows that a diet rich in antioxidants may help diabetics prevent the devastating cardiovascular, kidney, neurological and other damage that are common complications of diabetes."

The researchers recommend the regimen be tested in humans.

—D Dye

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