What's Hot

November 1999

What's Hot Archive


November 30, 1999

Vitamin E and Oat Fiber Prevent Risk of Heart Attack, Stroke

High-fiber foods or antioxidants such as vitamin E may help reduce the risk of heart attack or stroke following a meal high in fat.

At the annual meeting of the American College of Nutrition which took place in Washington, DC, Dr David L Katz of Yale School of Medicine presented the results of a study in which 50 healthy adults were fed high-fat (50 grams) meals once a week for three weeks, accompanied by either a bowl of oatmeal, whole-wheat cereal, or 800 IU vitamin E. Ultrasound measurements were taken of the diameter of each subject's blood vessels 3 hours before each meal and 3 hours after. Blood vessel diameter restriction is a risk factor for cardiovascular events and may also effect brain and sexual function. Blood vessels were restricted by 13.4% in those who consumed high-fat meals combined with whole-wheat cereal, yet vessel diameters were unchanged in those who received the vitamin E or oatmeal. Dr Katz provided the explanation that vitamin E helps quench free radicals resulting from metabolism which damage cells lining the blood vessels, impairing their ability to dilate in response to changes in blood flow thereby raising heart attack and stroke risk. The soluble fiber found in oatmeal helps prevent free radicals by preventing some of the absorption of fat and carbohydrate into the bloodstream. Foods such as vegetables, fruits and legumes contain moderate to high levels of soluble fiber but wheat contains insoluble fiber.

Dr Klatz recommends that ``we need to begin to pay attention not just to the health effects of diet over time, but the health effects of diet in short periods of time - including a single day or even a single meal.''

November 24, 1999

Fish Oil Supplements May Help People With Pancreatic Cancer

Cancer of the pancreas is the fifth leading cause of death from cancer in Western society. Less than 10% of patients survive a year afer diagnosis, and many suffer increasingly severe pain, nausea and vomiting, anorexia, weight loss, and weakness as the disease progresses.

It is possible that fish oil supplements may improve their condition as well as slow tumor growth. Studies have found that eicosapentanoic acid (EPA) - or fish oil, an omega-3 polyunsaturated fat, inhibits the growth of a variety of tumors in the laboratory. Also, EPA dietary supplementation has been shown to prevent general ill health and malnutrition, or cachexia. Based on the hypothesis that providing EPA in combination with calories and protein may result in weight gain rather than just weight stabilization, a nutritionally dense formula enriched with EPA has been developed.

A pilot study of 20 pancreatic cancer patients who had experienced weight loss was conducted by Dr Ken Fearon in Edinburgh to evaluate the nutrition supplement. Patients consumed a median of 1.9 237 mL servings of the supplement per day for three weeks. Before enrolling in the study patients had been losing an average of 3.2 kg/month and were severely malnourished. After supplementation they gained a mean weight of 1.1 ± .5 kg within three weeks and 2.5 kg within seven weeks. This weight gain is greater than that reported in the pure EPA studies.

Patients tolerated the product very well with only a few reports of gastrointestinal intolerance, which were mostly associated with pancreatic insufficiency and disease progression. Previous studies with EPA capsules reported problems with transient diarrhea and fishy taste and odor when burping. None of these problems were evident in this pilot study.

Researchers Judy Bauer and Dr Sandra Capra, from the Queensland University of Technology in Brisbane, Australia, have teamed up with a prospective, randomized, controlled, double blind multicenter trial involving 14 international sites. Ms Bauer is conducting an additional study which includes patients receiving chemotherapy. This study will be the first to use an oral nutrition supplement containing EPA in pancreatic cancer patients undergoing chemotherapy with gemcitabine. She believes the combination will have a synergistic effect on pancreatic cancer that is superior to the activity of either EPA or gemcitabine treatment alone.

November 22, 1999

Cancer Prevention With Phytochemicals and CLA

Phytochemicals are nonessential nutrients found in plant foods. They have potent cancer preventive effects that work by several mechanisms. Some phytochemicals improve the liver's detoxification capacity, so that more carcinogens can be neutralized and disposed of before they initiate cancer. Others block the effects of cancer-causing chemicals known as xenobiotics.

Heterocyclic amines, which are carcinogens formed during the cooking of meat and fish, cause cancerous changes in the colon and are thought to be a major contributing factor in colon cancer. In a recent study from the Linus Pauling Institute and Oregon State University, the potential of phytochemicals and other agents for blocking the cancer-causing effects of heterocyclic amines were studied. Researchers induced colon cancer in rats by giving them heterocyclic amines, then gave the animals various phytochemicals and other agents to see which ones were best at preventing cancer growth. The most effective inhibitors were found to be the indoles (found in cruciferous vegetables such as broccoli, cauliflower, and cabbage), catechins (found in green and black teas and berries), chlorophyllin (found in green vegetables), and conjugated linoleic acid (CLA). Indoles and catechins improve the liver's ability to detoxify carcinogens. Catechins are antioxidants that quench harmful free radicals. CLA increases interleukin-2 (IL-2) levels, which improves the body's resistance against cancer.

Xu M, Dashwood RH, "Chemoprevention studies of heterocyclic amine-induced colon carcinogenesis," Cancer Letters, 1999 Sep 1;143(2):179-83.

November 17, 1999

Gene Therapy Reverses Age-Related Memory Loss
by Angela Pirisi

Neuroscientists at the University of California, San Diego, are suggesting that gene therapy may actually reverse age-related memory loss. Published in the September 14 issue of the Proceedings of the National Academy of Science (PNAS), their research revealed that an age-related breakdown occurs in the subcortical system, a region that controls cortical and hippocampal activity. However, these brain cells do not die from age but are simply diminished in their capacity to function optimally. Usingrhesus monkeys to target the area, researchers essentially revived atrophied neurons and returned them to normal information-processing activity by implanting tissue grafts of genetically modified cells into that part of the brain to deliver nerve growth factor (NGF) to damaged, shrunken neurons.

The study comparatively analyzed the brains of young and old monkeys, and tissue-graft recipients versus non-treated aged monkeys. Results showed that the older monkeys (who were roughly equivalent to age seventy in humans) naturally had a 43% decline in the number of neurons in their subcortical region, as well as 10% shrinkage to the size of neurons. On the other hand, aged monkeys that had received grafts experienced a dramatic physical recovery and normal functioning of 92% of their neurons, along with the neuron size returning to within 3% range of normalcy.

These findings will have implications down the road for 4 million Alzheimer's patients, believe researchers, as well as addressing normal brain aging issues such as attention span, the ability to focus on several things at once, and general thought processing. According to lead researcher, Mark Tuszynski, M.D., Ph.D., associate professor of neurosciences at the University of California, San Diego School of Medicine, "These findings give us a new avenue to pursue in trying to enhance these functions in both the normal aged brain and in the diseased brain".

November 9, 1999

Acute Lymphocytic Leukemia May Be Prevented By Folic Acid

Researcher Martyn T. Smith of the University of California, Berkeley recently reported in the Proceedings of the National Academy of Sciences that a deficiency of folic acid may play a role in the development of acute lymphocytic leukemia. Dr Smith and his colleagues found that genetic mutations in the enzyme that processes folic acid may protect against this type of leukemia. Other research has shown that genetic mutations that specifically affect the processing of folic acid lessen the likeliness of the development of colon cancer.

The investigators analyzed blood samples from 308 adults with leukemia and 491 controls. Mutations in the gene for the enzyme that processes folic acid lowered the odds of having this type of cancer by three to fourteen times. The mutations did not offer protection against acute myeloid leukemia. According to Dr. Bruce N. Ames, also of the University of California, people who are not receiving adequate folic acid may be at risk for one type of leukemia. In the same issue of Proceedings, he editorializes that other nutrients and their effect on the development of cancer should be studied, observing that the rates of most cancers are double in those who consume the fewest fruits and vegetables compared to the rest of the rest of the population.

November 9, 1999

Vitamin K and Alzheimer's Disease

Dr. Martin Kolmeier of the University of North Carolina believes that vitamin K plays a role in Alzheimer's disease. Kohlmeier developed his theory after noticing that dialysis patients with a certain gene can't process vitamin K properly. That gene, known as apoE4, is prevalent in Alzheimer's patients. Alzheimer's patients with apoE4 are predisposed to having vitamin K deficiency.

Vitamin K activates special proteins in the brain that control calcium. It does the same thing in bone. Research shows that Alzheimer's patients have both porous bone and a lack of K-activated proteins in the brain.

Kohlmeier believes that vitamin K is the missing link between having the apoE4 gene and getting Alzheimer's. According to his research, apoE4 causes vitamin K to be cleared before the body has a chance to use it. That creates vitamin K deficiency in the body. And while it was previously thought that vitamin K's most important function was to help blood coagulate, new research indicates that the vitamin has many more important jobs in the body--such as maintaining bone. If Kohlmeier's theory is correct, people with the apoE4 gene are susceptible to Alzheimer's disease and vitamin K deficiency--and the two may be linked.

Kohlmeier M, et al. 1998. Bone fracture history and prospective bone fracture risk of hemodialysis patients are related to apolipoprotein E genotype. Calcif Tissue Int 62:278-81.

Saunders AM, et al. 1993. Association of apolipoprotein E allele e4 with late-onset familial and sporadic Alzheimer's disease. Neurology 43:1467-72.

November 2, 1999

Soy Aids Vascular Function of Postmenopausal Women

The North American Menopause Society's yearly meeting, held in New York, was the site of a presentation by the authors of a study which demonstrated that the intake of soy isoflavones can improve vascular function by improving endothelial function. The endothelium is a layer of flat cells lining blood and lymphatic vessels, and the heart. Menopause marks the onset of increased cardiovascular disease risk in women because the decline of estrogen has been linked to an increase in endothelial dysfunction. This is preventable in part by estrogen replacement therapy, but the side effects involved with ERT preclude its use by some women. The study, presented by Dr Robert DuBroff and Dr P Decker of Southwest Cardiology Associates in Albuquerque, New Mexico, reported the findings in postmenopausal women who consumed forty grams per day of soy protein containing 88 mg isoflavones. Upon examination by brachial artery ultrasound, the women were found to have improved endothelial function. The intake of soy isoflavones may be a viable replacement for estrogen in postmenopausal women in regard to the prevention of cardiovascular disease as well as for prevention of other menopausal symptoms.

November 2, 1999

Chill Out This Winter and Survive The Holidays

Holiday celebrating and stress could increase the risk of a fatal heart attack. Analyzing more than 200,000 death certificates from 1985 through 1996, researchers at the University of Southern California discovered an increase in deaths from coronary artery disease starting after Thanksgiving and peaking around New Year's. The data showed cardiac deaths occurred 33 percent more often during the this annual period of festivity than during the summer and early fall.

Physicians attribute the seasonal bump to holiday stress and the consumption of tempting high-fat foods, alcohol and salt. In addition, the researchers speculate that particles given off by wood-burning fireplaces could contribute to the deaths by irritating lung tissue, which decreases available oxygen and stresses the heart. Respiratory infections, more prevalent in the winter, could be another factor.

A few previous studies indicated the number of cardiac deaths climb in the morning and when temperatures drop. The heart works harder in cooler temperatures, and blood pressure and the clotting protein fibrinogen rise. But this study indicates the seasonal correlation exists even in southern California's mild climate, where temperature variances are insignificant.

Author Dr. Robert A. Kloner recommends cutting back on the high-fat foods during the holidays. The U.S Departments of Agriculture and Health and Human Services advise limiting fat intake to 30 percent of calories consumed and saturated fats to less than 10 percent.

Chilling out and not letting the holidays add to life's pressures might help, too. A recent study reported in the American Journal of Clinical Nutrition suggests that prolonged stress raises levels of blood lipids and lipoproteins. Senior author Dr. Jean Dallongeville says the study shows mental stress increases fat levels and decreases the rate fats clear the blood after meals. When lipids stay longer in the system, cardiovascular risk climbs.

Circulation: Journal of the American Heart Association. 1999;100:1630-1634, http://circ.ahajournals.org/cgi/content/abstract/100/15/1630


November 1, 1999

Antimicrobial Treatment Aids Gum Sufferers,
Lowers Disease Risk

People keep their natural teeth longer than in the past. But with age, gum disease becomes more prevalent. New antimicrobial approaches to periodontal treatment can prevent extractions and spare patients painful gum surgery.

Professor Walter L. Loesche of the University of Michigan School of Dentistry reports in Critical Reviews of Oral Biology and Medicine that antimicrobial therapy reduces the disease's cause, while traditional surgery to remove inflamed tissue reduces the result of periodontal infection.

Researchers have determined the bacteria responsible for gum problems and identified specific agents that will suppress or eliminate the infection. Recommended antibiotic treatment varies depending on the severity of the problem. Some patients will need a combination of traditional scraping and planing with a one- or two-week course of pills. For those with gum disease involving just a few teeth, clinicians can apply an antibiotic gel, chip or film into the deep pockets that develop between the teeth and gums. Loesche warns that antibiotics should be used only for confirmed bacterial infections serious enough to warrant treatment.

Several studies have linked gum disease to systemic conditions, including heart disease and diabetes mellitus. Controlling the bacteria, so it does not provoke an inflammatory response, could reduce heart attack and stroke risk, and improve blood sugar control. The results of one study lead its investigators, Dr James D. Beck and Dr Steven Offenbacher, to conclude that individuals with severe periodontal bone loss may have twice the risk of fatal coronary heart disease as normal individuals. "Establishing periodontal diseases as a risk factor for heart disease and stroke would take on new meaning for oral health as it relates to the overall health of individuals," stated Drs Beck and Offenbacher.

Critical Reviews of Oral Biology and Medicine (Volume 10, issue 3, 1999)


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