Lower dose of garlic extract more effective
In a report published in the May 31, 2006 issue of the Journal of Agricultural and Food Chemistry, Shela Gorinstein and her colleagues in Israel and Poland revealed that a lower dose of a garlic extract appears to be more effective than higher doses to lower cholesterol and help protect against excessive blood clotting. Garlic extract has been found to be helpful for several conditions, but the odor it imparts to its users has made taking higher doses undesirable for some people.
Dr Gorinstein's team fed rats diets containing 1 percent cholesterol to four groups of rats. Three groups also received a commercial garlic extract equal to 500, 750 and 1000 milligrams raw garlic per kilogram body weight. A control group was provided with a diet to which cholesterol and garlic were not added. The polyphenols and antioxidant potential of the extract were evaluated prior to its administration. Plasma lipids, fibrinogen (involved in blood clotting), clotting time, and antioxidant capacity were measured before and after the four week treatment period.
At the end of the study, all of the rats on the diets to which cholesterol was added experienced a decrease in plasma antioxidant activities, yet the decrease among rats who received the 500 mg/kg garlic-enhanced diets was not considered significant compared to the control group. Only the rats who received 500 mg experienced a significantly reduced rise in plasma lipids. The same group also showed a significant decrease in plasma fibrinogen and an increase in clotting time.
The amount of fresh garlic that a human would need to consume to be equivalent to the 500 milligram dosage is 1.25 ounces per day for a 150 pound person, which would be supplied by eating about 12 cloves. The authors concluded that "commercial garlic could be a valuable component of atherosclerosis-preventing diets only in optimal doses."
St John's wort beats bladder pain
The results of a study presented on May 23, 2006 at the American Urological Association's annual meeting found that the herb St. John's wort could be helpful to relieve the pain of hypersensitive bladder disorders such as interstitial cystitis, a condition that affects an estimated 700,000 Americans, the majority of whom are women.
Reduced lung function found in vitamin D deficient teens
The results of a study of over 2,000 teens aged 16 to 19 presented at the American Thoracic Society International Conference on May 22, 2006 found that those whose intake of vitamin D was low had poorer lung function than those whose diets met the recommended amount. The vitamin is found in dairy products, egg yolks, saltwater fish, and in many calcium and multivitamin supplements. The recommended daily allowance of vitamin D for this age group is 200 international units, which is less than what many authorities consider optimal. Jane Burns, ScD, who is a research fellow at the Department of Environmental Health at the Harvard University School of Public Health in Boston, decided to study adolescents because of their notoriously poor eating habits. Dr Burns and her colleagues found that 35 percent of the 2,112 adolescents studied consumed 157 international units or less vitamin D per day. The researchers found similar results for both boys and girls.
"These are adolescents who should have optimal pulmonary function," Dr Burns stated . "If they're already showing lower pulmonary function associated with lower vitamin D intake at this age, it may have long-term effects on their health."
"Vitamin D is promoted in terms of bone growth, but we also need to think in terms of vitamin D's other effects on the body," Dr. Burns adde d. "It may be that we should be promoting dietary vitamin D intake at recommended levels to ensure optimal lung function as well as to form and maintain healthy bones ."
"We don't know by which mechanism vitamin D affects pulmonary function--it's an area that needs to be explored," she noted.
Scientists turn vitamin E into super cancer killer
A report published in the April 28 issue of the Journal of Biological Chemistry detailed the discovery of researchers at The Ohio State University Comprehensive Cancer Center-Arthur G. James Center Hospital and Richard J. Solove Research Institute that slightly modifying alpha-tocopherol (vitamin E) succinate makes its cancer killing ability five to ten times greater than that of the vitamin in its normal state. Vitamin E succinate has already been shown to induce programmed cell death in cancer cells, but researchers had been unaware of how it causes this to occur.
“Overall, out findings are proof of the principle that this drug can kill cancer cells very effectively but does very little damage to healthy cells,” he concluded.
Oxidative damage to mitochondrial proposed as possible cause of Parkinson's disease
A report published in the May 10, 2006 issue of the Journal of Neuroscience concluded that oxidative damage to the mitochondria of the brain's cells from internal processes could be one of the main causes of Parkinson's disease (PD). Mitochondria are organelles within the cells that are responsible for generating energy.
Neuroscientists at the University of Virginia Health System compared the brains of ten deceased Parkinson's patients to those of twelve normal individuals matched for age. The diseased brains were found to have 50 percent more damage from oxygen free radicals to a mitochondrial protein structure known as complex I, which is the first stop in the electron transport chain that produces an electrical charged used to make energy. Lead researcher Dr Jim Bennett, who is neurologist at the University of Virginia, stated, "This part of the protein complex is being damaged by oxygen free radicals more in a brain with Parkinson's than it is in someone of same age who does not have PD. If this damage is caught in people early on, we might interrupt the progression of Parkinson's disease. Such treatment is hypothetical at this point, but it is rational."
At this point, Dr Bennett's team does not yet know why complex 1 is damaged in Parkinson's disease patients. "It could be that something has gone terribly wrong with the mitochondrial genome passed down by a person's mother that codes for several proteins in complex I," he suggested. "Something could be wrong in the coding for genes that help complex I assemble. Or there could be environmental toxins. Our research is a first real step in understanding at a detailed biochemical level what the challenge is."
Combined vitamin C and E deficiency results severe central nervous system damage in a matter of days
An article published in the June, 2006 issue of the Journal of Nutrition detailed the findings of researchers at Vanderbilt University in Nashville, Tennessee that giving guinea pigs diets that are deficient in vitamin C and vitamin E results in severe central nervous system damage within 5 to 15 days.
Because most animals make their own vitamin C, the current study used guinea pigs that, like humans, cannot manufacture vitamin C, and are therefore susceptible to becoming deficient in the vitamin. Sixteen guinea pigs were fed vitamin E deficient diets and 8 animals were fed diets with adequate vitamin E for two weeks, following which each group was divided to receive either a vitamin C deficient or replete diet in combination with their previous regimens.
From the fifth day after beginning the vitamin C deficient diets, 9 guinea pigs out of the 12 who received diets deficient in both vitamins C and E experienced hind leg weakness or paralysis, and two of the animals died between the tenth and eleventh days. Only one guinea pig in this group survived 15 days. None of the animals in the other three groups showed any signs of neurological damage, and examination of the animals' brains and spinal cords confirmed that only guinea pigs with combined deficiencies had central nervous system damage, including nerve cell death, axonal degeneration, and vascular injury.
The authors suggest that blood vessel injury may have been the primary cause of the central nervous system injury observed in the paralyzed animals. They note that some of the effects observed in experiments involving vitamin C or vitamin E deficiency alone were seen in the current study; the difference being that "the double deficiency quickly produces lethal effects, whereas the single deficiencies require longer times to produce their lesser effects."
Over 80 million Americans risk early death due to controllable conditions
America’s bad habits are putting many of its citizens at risk of dying early, according to the British Medical Journal’s May 12, 2006 issue. Professor of Clinical Public Health Cheryl G. Healton at Columbia University and her colleagues at the American Legacy Foundation evaluated data from 29,305 adults over the age of eighteen who took part in the 2002 national health interview survey to estimate the proportion of Americans who smoke or are obese, factors that are known to increase disease risk and early death. The results were stratified for age, gender, ethnic origin, education, and income.
The team calculated that 23.5 percent of American adults were obese and 22.7 percent smoked. Approximately 9 million Americans (4.7 percent) were obese and smoked, in contrast with the common perception that smokers are thinner. African Americans and individuals whose income and education levels were lower had the greatest proportion of combined smoking and obesity of all groups examined. Since obesity and smoking are already well established as hindrances to a long and healthy life, the combination could have a significant impact on life span.
Previous research has found that men and women who stop smoking gain an average of 2.8 to 5 kilograms, which can persist in some individuals. It is unknown whether people who are both obese and smokers are more or less likely to gain weight, nor how efforts to lose weight affect their smoking cessation efforts.
In an era of increased longevity in a western country known for its advanced healthcare, it is ironic that a significant portion of the population is at risk of early death due to factors that are self-inflicted. The authors recommend that research be conducted to investigate treatments for people who smoke and are obese.
Soy isoflavones improve postmenopausal women's immune function and lower oxidative damage
A report published in the May 2006 issue of the American Journal of Clinical Nutrition revealed that consuming soy isoflavones for four months resulted in higher B cell counts and a reduction in DNA damage in a group of postmenopausal women.
Fifty-two women between the ages of 50 and 65 were assigned to receive cow's milk plus a placebo supplement, soymilk (providing 71.6 mg isoflavones) plus a placebo supplement, or cow's milk plus a 70 milligram isoflavone supplement daily for sixteen weeks. Blood and urine samples were analyzed at the beginning and conclusion of the study for lymphocyte (white blood cell) subsets, cytokines, and inflammation and oxidative damage markers.
At the end of the study, plasma concentrations of the isoflavone genistein were significantly higher in women who received soymilk or isoflavone supplements than than in those who received the cow's milk/placebo combination. Although women who received isoflavones did not experience an increase in such factors as gamma interferon or interleukin 2, white blood cells known as B lymphocytes were higher among women who received either form of soy than in those who did not receive soy, with subjects who received the isoflavone supplement experiencing the greatest increase. Plasma 8-hydroxy-2-deoxy-guanosine, a marker of oxidative DNA damage, was lower in women who received the two soy-containing regimens than among those who received no soy.
The authors discuss the fact that isoflavones have nonhormonal properties that can benefit older individuals, particularly their ability to function as antioxidants and protect against diseases that result from oxidative damage. They note that the increase in B cells in response to the estrogenic action of isoflavones is in agreement with earlier studies that have shown that estrogen enhanced humoral immunity. They recommend research to determine the effect of soy isoflavones in immunologically challenged individuals.
Little things mean a lot
A study published in the March, 2006 issue of Antioxidants and Redox Signaling found that animals whose calories were restricted by just 8 percent and who engaged in light exercise experienced an increased average life span and a reduction in the cellular damage that occurs with aging. Although restricting calories by 20 to 40 percent has been well established as a method to increase life span, most humans find it difficult to duplicate this degree of dietary restriction.
Scientists at the University of Florida's Institute on Aging in Gainesville compared four groups of rats: old rats who had received a diet that allowed them to eat all they wanted, old rats who received a diet that contained 8 percent fewer calories than the unlimited diet, old rats who received the 8% calorie restricted diet plus access to an exercise wheel, and young rats on non-restricted diets. (An 8 percent reduction is the human equivalent of a few hundred calories.)
When rats on non-restricted diets were compared, levels of reactive oxygen species and peroxynitrite were higher in the older animals, while the antioxidant glutathione was lower. The calorie restricted groups lived longer on average than rats allowed to eat as much as they desired. By evaluating damage to liver RNA and DNA, the team found more age-asociated damage to RNA than DNA in the non-restricted older rats, suggesting that RNA could be useful as an aging biomarker.
Senior author and University of Florida College of Medicine associate professor of aging and geriatric research Christiaan Leeuwenburgh, PhD, stated, "This finding suggests that even slight moderation in intake of calories and a moderate exercise program is beneficial to a key organ such as the liver, which shows significant signs of dysfunction in the aging process."
Resveratrol reduces colon tumor formation in animal model
The May 5, 2006 issue of the journal Carcinogenesis published the findings of researchers at Annamalai University in India that rats fed trans-resveratrol experienced reduced colon tumor formation in response to the carcinogen 1,2-dimethylhydrazine (DMH) compared to rats who did not receive the protective compound.
Namasivayam Nalini and colleagues divided 96 rats into six groups, four of which received weekly injections of DMH for fifteen weeks. Three groups of rats who received the carcinogen and one of the control groups were administered 8 milligrams per kilogram body weight oral resveratrol daily at various stages throughout the thirty week study.
At the end of the study, animals who received resveratrol and DMH were better able to maintain their growth rate and weight than the group that received the carcinogen without resveratrol. When the animals' colons were examined, tumors among rats who received resveratrol were fewer and smaller, with a lower histological degree and depth of involvement. Large intestinal adenocarcinomas, which made up 63 percent of the tumors in rats who received DMH alone, were reduced to zero in the group of rats who received resveratrol throughout the entire study period. Aberrant crypt foci, which are precancerous lesions that have been found in humans with a high risk of developing colon cancer, were also significantly lower among rats who received resveratrol.
The protective effect of resveratrol on the development of colon cancer may be due its antioxidant activity. Resveratrol was associated with greater superoxide dismutase, catalase and glutathione peroxidase activity in the liver and colon of DMH-treated rats compared to levels measured in rats who did not receive resveratrol. The authors conclude that resveratrol "might have practical applications as a chemopreventive agent, providing a scientific basis against human colon carcinogenesis."
Higher carotenoid levels associated with reduced diabetes risk in nonsmokers
The May 15, 2006 issue of the American Journal of Epidemiology reported findings obtained among 4,493 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study that having higher levels of serum carotenoids is linked to a lower risk of developing diabetes and insulin resistance, but only in nonsmokers. Carotenoids are nutritional compounds found in plants that decrease oxidation by quenching free radicals and singlet oxygen. Oxidative stress is believed to play a role in the development of diabetes and other diseases.
The CARDIA Study included men and women aged 18 to 30 years living in the United States. Participants were examined upon enrollment between 1985 and 1986 and at five follow-up examinations spanning 15 years. An ancillary study (the Young Adult Longitudinal Trends in Antioxidants study) measured serum carotenoid concentrations (alpha-carotene, beta-carotene, lycopene, lutein plus zeaxanthin, and beta-cryptoxanthin) in the majority of CARDIA subjects at the beginning of the study and at the seven year follow-up examination.
Thirty-four percent of the subjects were smokers. There were 148 cases of diabetes diagnosed over the fifteen-year follow-up period. Having higher total serum carotenoid concentrations was inversely associated with a diabetes risk, insulin levels, and insulin resistance only among nonsmoking participants.
The authors remark that even with high concentrations of serum antioxidants, tissue levels may still be lower in smokers due to increased oxidative stress. Oxidative stress caused by smoking may overwhelm the carotenoids' antioxidant activity. Alternatively, smoking could alter beta-carotene metabolism, which can affect cellular activity, and, in turn, diabetes risk.
Although the findings of the study support the hypothesis that carotenoids may oppose oxidative stress and the occurrence of diabetes, they conclude that their observations support "the concept that antioxidant metabolism and the oxidative defense system behave differently in smokers than in nonsmokers."
Vitamin A and C synergistically fight breast cancer cell growth
A study published in the Journal of Nutritional Biochemistry found that administering both vitamin A and vitamin C to cultured human breast cancer cells was more than three times as effective than the administration of either compound alone.
Korean researchers cultured a commonly used human breast cancer cell line for three days with five different concentrations of retinoic acid (vitamin A), four concentrations of ascorbic acid (vitamin C), or both compounds, then counted the number of cells. They found that while cell proliferation was inhibited by 20.7 in response to 100 nanomoles per liter retinoic acid, and by 23.3 percent with 1 millimole ascorbic acid, the combination of the two vitamins inhibited proliferation by 75.7 percent compared to untreated cells.
Microarray analysis detected the upregulation of 29 genes and down-regulation of 38 genes with the combined vitamin treatment. Among upregulated genes were those involved in differentiation, proliferation inhibition, apoptosis, cell cycle regulation, and antioxidation (including upregulation of glutathione S-transferase and superoxide dismutase). Down-regulated genes included insulin-like growth factor-binding protein 5.
Vitamins A and C are among several that have been associated with a reduction in breast cancer risk in epidemiologic studies. The ability of retinoic acid to inhibit tumor cell proliferation is well known, although its mechanism has not been defined. The authors suggest that the synergistic effect observed in this study is due to ascorbic acid's ability to slow the degradation of retinoic acid, thereby increasing vitamin A's cell proliferation inhibitory effects.
"This is the first time the effect of combining retinoic and ascorbic acid on breast cancer cell proliferation, differentiation, apoptosis and antioxidant-related gene expression has been studied," the Korean team announced. Further analysis is recommended to aid the design of better anticancer treatments.
Increased polyunsaturated fats and vitamin E intake associated with lower ALS risk
A report published online in the Journal of Neurology, Neurosurgery and Psychiatry revealed an association between a higher intake of polyunsaturated fats and vitamin E with a reduced risk of developing the motor neurone disease amyotrophic lateral sclerosis (ALS). Polyunsaturated fats include omega-3 and omega-6 fatty acids.
For the current study, researchers in the Netherlands compared 132 patients with potential or definite ALS with 220 healthy controls. Responses to food frequency questionnaires concerning nutritional intake before the onset of the disease were used to determine the intake level of a number of nutritional components including energy, fats, cholesterol, vitamin C, vitamin E and calcium.
Although the amount of energy consumed daily was the same for both groups, ALS patients had a significantly lower intake of polyunsaturated fatty acids and vitamin E. For subjects whose polyunsaturated fatty acid intake was over 32 grams per day, there was a 60 percent lower risk of developing ALS than that experienced by individuals whose intake was less than 18 grams. Having an intake of vitamin E of 18 to 22 milligrams compared to less than 18 milligrams per day was associated with a similar reduction in risk. Interaction analysis showed that polyunsaturated fatty acids appear to work synergistically with vitamin E to help prevent ALS.
The findings are consistent with those of a previous study that revealed a 40 to 50 percent reduced risk of developing ALS among regular users of vitamin E supplements. Additionally, omega-3 polyunsaturated fatty acids have been shown to help protect against inflammation, a pathological process which has been observed in the disease. Vitamin E may help reduce ALS risk directly via preventing lipid peroxidation and may also act indirectly by making higher levels of polyunsaturated fatty acids available by inhibiting their peroxidation.