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.

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.

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.

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."

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

A report published in the April 21, 2006 issue of the Journal of Biological Chemistry revealed the findings of Emory University School of Medicine researchers that a protein known as DJ-1, which, when mutated, results in hereditary Parkinson's disease, is also involved in nonhereditary (sporadic) Parkinson's disease when it becomes damaged by oxidative stress. Approximately 90 percent of Parkinson's disease cases are believed to be nonhereditary. "One popular theory has suggested that these sporadic cases result from exposure to environmental toxins, such as herbicides or pesticides," lead author and associate professor of pharmacology Lian Li, PhD, observed. "Previous research has indicated that these toxins lead to oxidative stress. While oxidative stress does occur naturally as humans age, further oxidation caused by toxins may overwhelm the body's antioxidants. This theory has been around for a long time. But what's been damaged by this oxidative stress?"

Doctor Li's team examined DJ-1 oxidation levels in the brains of individuals with nonhereditary Parkinson's and Alzheimer's disease, and age-matched controls and found that the protein showed signs of oxidative damage in the brains of the diseased patients. As in hereditary Parkinson's, structural changes to the protein leads to its loss and degradation. "The protein unfolds and cannot function normally," Dr Li explained. "Not recognizing the unfamiliar shape, the protein is broken down by the cell. The end result is the same: you lose your protein. Any mutation or modification causing this protein to lose its function will then lead to neurodegeneration in Parkinson's disease."

Dr Li is researching the possibility that DJ-1 could function as an antioxidant, leaving the cell vulnerable to oxidative damage when the protein is mutated. Until drugs are developed that target DJ-1, Dr Li notes that green tea and vitamin C are good dietary sources of antioxidants.

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.

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.