Majority of children need more fiber
The results of a study published in the February 2005 issue of the Journal of the American Dietetic Association indicate that over 75 percent of preschool aged children may be failing to obtain adequate fiber in their diets.
Researchers from Penn State led by assistant professor of nutritional sciences Dr Sibylle Kranz analyzed the diets of 2,805 2 to 3 year old and 2,632 children between the ages of 4 and 5. Dietary information was provided by the children's parents via surveys conducted by the U.S. Department of Agriculture.
Dr Kranz and colleagues found that the majority of the children did not meet the new National Academy of Sciences Dietary Reference Intake level of 14 grams fiber per every 1000 calories consumed--an amount believed to help reduce cardiovascular disease risk. Those whose fiber intake was in the top one-fourth of participants consumed a greater quantity of nutrient dense foods.
Dr Kranz commented, "There is clinical evidence that children with low fiber intakes are at risk of chronic constipation. However, there are also other reasons to encourage fiber consumption in children. For example, fiber has been shown to lower cardiovascular risk in adults. Children who eat high-fiber foods are more likely to grow up into adults who consume adequate fiber."
"If parents feed their preschoolers fiber-rich foods, they are most likely providing important nutrients for the children as well," Dr Kranz added. "An easy substitution to get more fiber into their diets is to change to whole-grain products and high-fiber cereals. Also, children usually like sweet potato, baked beans, grapes and oranges and they're all high-fiber, high-nutrient foods."
Increased calcium from supplements and diet lowers women’s colorectal cancer risk
The January 2005 issue of Cancer Epidemiology, Biomarkers and Prevention (http://cebp.aacrjournals.org/) published the findings of a University of Minnesota Cancer Center study that women who consumed high calcium diets as well as higher amounts of calcium from supplements experienced a 46 percent lower risk of developing colorectal cancer than women whose intake from both sources was lower.
The study, conducted by University of Minnesota Cancer Center and School of Public Health epidemiologist Andrew Flood, PhD, and researchers at the National Cancer Institute, enrolled 45,354 women who had participated in the Breast Cancer Detection Demonstration Project. The women completed questionnaires which provided information on dietary calcium and the use of supplements. During the 8.5 year follow-up period, 482 women developed colorectal cancer.
When calcium from dietary sources alone was examined, it was found that women whose intake was in the top one-fifth of participants at over 830 milligrams per day had a 26 percent lower risk of developing colorectal cancer than women whose intake was in the lowest fifth. Women whose calcium supplements provided 800 milligrams or more of the mineral per day experienced a 24 percent lower risk of developing colorectal cancer than women who did not use calcium supplements. However, when calcium from both diet and supplements was high, colorectal cancer risk dropped to 46 percent lower than the risk experienced by women whose dietary calcium was lower and whose supplemental intake was less than 800 milligrams.
Dr Flood remarked, "It is especially notable that the risk reduction was present regardless of the source of the calcium, and that simultaneously consuming high levels of calcium from both diet and supplements further reduced risk. These observations suggest that it was the calcium per se, and not merely dairy products or some other variable that accounted for the reduction in risk."
Osteoporosis prevention starts in childhood
A study published in the January 2005 issue of the American Journal of Clinical Nutrition found that supplementing with calcium increased the bone mass of prepubertal girls, which not only improved their current health status but helped protect against the risk of developing osteoporosis later in life. Osteoporosis is a disease that occurs in many older women which is characterized by a reduction in bone density.
In the first longterm clinical trial to evaluate the effect of calcium supplements on bone density in girls ages 8 to 13, researchers from Ohio State University Medical Center divided 354 girls to receive supplementation with 670 milligrams calcium per day or a placebo for four years. Participants had the option of remaining in the trial for an additional 3 years. The girls’ diets provided an average of 830 milligrams calcium per day. Bone mineral density of the wrist, elbow, hand and total body were determined upon enrollment, and at 4 and 7 years.
It was discovered that calcium supplementation had the most significant impact on bone density during the prepubertal growth spurt, and that its effects decreased after the onset of menstruation. Bone mineral density in all areas measured was significantly greater after 4 years in the supplemented group than in those who received the placebo, but the effect was found to have diminished at the 7 year point. Lead author and director of the Osteoporosis Prevention and Treatment Center at Ohio State, Velimir Matkovic, commented the findings: “Because most bone mass is accumulated during this phase of growth, preadolescence may represent the time of highest need for calcium in a female’s lifetime . . . The importance of preventing osteoporosis can’t be overstated. Prevention of this disease will not only improve the population’s quality of life, but will also undoubtedly save on the skyrocketing health care costs associated with treatment.”
Type of fat more important than amount
A study published in the American Medical Association journal Archives of Internal Medicine (http://archinte.ama-assn.org) found that when considering dietary fats, quality is more important than quantity.
Diets low in fat have been shown to help reduce cardiovascular disease risk factors. Polyunsaturated fats have been recommended over saturated fats for several decades, but the existence of relatively few studies supporting this recommendation has caused it to be questioned by some health and medical authorities. Some studies have shown that polyunsaturated fats lower serum low-density lipoprotein (LDL) cholesterol, while saturated fats increase it.
David E. Laaksonen, MD, PhD, from University of Kuopio, Finland, and colleagues evaluated the intake of the polyunsaturated fat linoleic acid, found in flax and other plant oils, as well as total polyunsaturated fat intake, for 1,551 middle aged Finnish men. Four day food records and blood tests were used to estimate dietary fatty acid intake. The participants were followed for 15 years.
During follow-up there were 225 deaths, 78 which were caused by cardiovascular disease. The research team found that men whose serum linoleic acid, omega-6 fatty acids and total polyunsaturated fatty acids were in the top one-third of participants were three times less likely to die of cardiovascular disease than those whose intake was in the lowest third. Assessment of dietary intake found that linoleic acid and total polyunsaturated fatty acid intake was inversely associated with cardiovascular disease mortality. Total fat intake was not related to cardiovascular disease or all-cause mortality.
The authors conclude, "Dietary fat quality thus seems more important than fat quantity in the reduction of CVD mortality in middle-aged men. Carrying out recommendations to replace saturated fat with polyunsaturated fat in the primary prevention of cardiovascular disease may substantially decrease CVD and to a lesser degree overall mortality."
American Cancer Society’s latest report shows cancer deaths lead heart disease in people under 85
A report published in the January/February 2005 issue of the journal CA: A Journal for Clinicians revealed that since 1999 cancer has surpassed heart disease as the leading cause of death in the United States among men and women under the age of 85. The report, entitled Cancer Statistics 2005, examines mortality data obtained from the National Center for Health Statistics and cancer incidence and survival statistics from the National Cancer Institute.
Deaths from cancer in Americans under the age of 85 in 2002 totaled 476,009, compared to 450,637 deaths from heart disease in this age group. However, the rate of death for all cancers combined actually decreased, albeit slightly, by 1.5 percent percent per year between 1993 and 2001 in men and by 0.8 percent per year in women. The cause behind cancer’s taking the lead is the decline in heart disease deaths that has occurred over the past decades. When the population including those over age 85 was examined, heart disease still ranked as the number one killer in this country.
While the incidence of many cancers has slowed, prostate and breast cancer rates continue to rise. The authors attribute breast cancer’s increased incidence to the increased prevalence of obesity and the use of hormone replacement therapy among women.
The report also predicts this year’s cancer incidence and deaths, with approximately 1.4 million new cases of invasive cancer anticipated, and 570,280 deaths from the disease.
Of interest was the attribution of exposure to infectious agents such as hepatitis B and C, human papilloma virus and H pylori as the primary cause of the increased incidence of several types of cancer in various groups studied. Perhaps future cancer research will one day identify other infectious causes of this national epidemic.
Folate from diet and supplements lowers hypertension risk
The January 19 2005 issue of the Journal of the American Medical Association (JAMA) published the findings of Harvard researchers led by John P. Forman that intake of the B vitamin folate is inversely related to the risk of hypertension in women.
Dr Forman and colleagues examined data obtained from the Nurses Health Study I, which enrolled women aged 43 to 70, and the Nurses’ Health Study II, which included women between the ages of 27 to 44. Data from 53,739 participants in the Nurses’ Health Study I and 88,999 women in the Nurses’ Health Study II were selected for the current analysis.
During the eight year follow-up period, 12,347 cases of hypertension were diagnosed in the Nurses’ Health Study I, and 7,373 in the Nurses’ Health Study II. Older women (in the Nurses’ Health Study I) whose intake of folate from diet and supplements was 1000 micrograms per day or greater experienced an 18 percent lower risk of developing hypertension than those whose intake was less than 200 micrograms. For the younger women in the Nurses’ Health Study II whose folate intake was 1000 micrograms or more, the risk of hypertension was 46 percent lower than that of women with the lowest intake. When folate from diet alone was analyzed, no significant effect was found, possibly because few participants consumed high quantities of foods containing the vitamin, however the authors offer a secondary explanation that supplemental folic acid has twice the bioavailability of that which naturally occurs in food.
To the authors’ knowledge, the study is the first to report an association between folate intake and hypertension risk. Supplemental folic acid’s ability to improve endothelial function has been demonstrated in several studies, which could provide an explanation for its protective effect.
Seizure drugs linked to longer life in roundworms
In yet another study involving the lowly but lucky roundworm C elegans, geneticist Kerry Kornfield and colleagues from Washington University School of Medicine in St Louis, Missouri discovered that the anticonvulsant drugs ethosuximide, trimethadione and 3,3-diethyl-2-pyrrolidionone (DEABL) increased the worms’ mean and maximum lifespan. The findings were published in the January 14 2005 issue of the journal Science.
By screening three doses of 19 classes of drugs using 50 worms for each, the team discovered that a moderate dose of the anticonvulsant drug ethosuximide extended the mean adult lifespan of the roundworms by 17 percent at 20 degrees Celsius. When the related drug trimethadione was tried, mean lifespan increased by up to 47 percent and a 57 percent extension of maximum lifespan was observed. Another drug in this category, DEABL, also extended lifespan, but to a lesser extent.
Although the drugs’ mechanism of action in extending life span is not yet known, they appear to stimulate the neuromuscular system of the worms, and affect neurons involved with egg laying and body movement, leading the worms to lay their eggs earlier and to become more active. Analysis of the treated worms’ stages of aging indicated “that ethosuximide and trimethadione delay the aging process.”
Unlike genetic mutations that have been found to extend the lifespan of these roundworms, the anticonvulsant drugs don’t act through the insulin-like signaling system. Dr Kornfield commented, “We think the nervous system effects are more complicated than simply regulating insulin signaling. The nervous system might have a central function in coordinating the progress of an animal through its life stages leading ultimately to degeneration.”
“It’s very early days for understanding the connection between neural function and aging,” he concluded.
Iron deficiency reprograms cellular genetic expression
A study reported in the January 14, 2005, issue of the journal Cell has found that a deficiency of iron altered the expression of over 80 genes in yeast cells. Iron is an essential mineral, and too much or too little can have lethal consequences.
Professor of Pharmacology and Cancer Biology Dennis J. Thiele, PhD, and colleagues at the Sarah W. Stedman Nutrition and Metabolism Center at Duke University Medical Center demonstrated for the first time what occurs within a cell when it lacks iron. The team used yeast cells because of the similarity of their genome to that of humans. They demonstrated that the cells shut down the major users of iron in order to maintain the cells’ essential functions.
Dr Thele and colleagues found that a protein known as Cth2 is overproduced by iron deficient cells. Cth2 binds to the messenger RNA of over 80 genes and targets it for degradation or destruction, which prevents these genes from performing their roles. While some of the genes affected by Cth2 are known to be involved in generating energy, copying the cell's genetic code and protecting the cell from free radicals and aging, the function of many is unknown, leading to speculation that many of iron deficiency’s effects are not being attributed to the condition.
Dr Thiele summarized, "We discovered that iron deprivation actually reprograms the metabolism of the entire cell. Literally hundreds of proteins require iron to carry out their proper function, so without this nutrient, there is a complete reorganization of how cellular processes occur.”
He added, "Current diagnostic markers for iron deficiency aren't very sensitive, unless the deficiency is severe. Pinpointing the genes affected by iron deprivation should provide us with a genetic fingerprint of what patients with varying levels of iron deprivation look like."
Another study in mice shows calorie restriction helps prevent Alzheimer’s
Readers of “What’s Hot” on December 15 2004 will recall a study in which Caleb E Finch and colleagues found a reduction of the plaques that characterize Alzheimer’s disease (AD) in mice whose diets were restricted in their number of calories. Now, researchers from Mount Sinai School of Medicine have produced similar findings in a study that involved calorie restriction achieved by reducing the amount of carbohydrates in the animals’ diets. The report is scheduled to be published in the Journal of the Federation of American Societies for Experimental Biology (FASEB).
Researchers led by Mt Sinai professor of Psychiatry, Neurosciences and Geriatrics, and Adult Development, Giulio M Pasinetti MD, PhD, allowed one group of mice bred to develop amyloid plaques to eat as much as they wanted, and provided another group of the mice with a diet that provided 30 percent fewer calories. The diets were begun at three months of age, and the animals were evaluated at one year for the presence of amyloid plaques.
While all of the mice who consumed unlimited calories developed amyloid plaques, the mice who received the restricted diets had almost no evidence of plaque formation. It was discovered that antiamyloidgenic activities were increased in the calorie restricted mice, meaning that the diet activated pathways that break down amyloid beta peptides in the brain before plaques are formed.
Dr Pasinetti commented, "This rather mild change in diet resulted in a remarkable measure of disease prevention. There is epidemiological evidence that humans who consume reduced calorie diets have a lower incidence of AD. Our investigation provides a possible rational for this observation and possible mechanisms through which caloric reduction may provide protection in Alzheimer's disease."
CLA helps protect against nonalcoholic fatty liver disease
The January 1 2005 issue of the Journal of Nutrition published the findings of researchers from Saga University in Japan that the dietary supplement conjugated linoleic acid (CLA) protected against nonalcoholic fatty liver disease in rats bred to develop the condition.
Twelve Zucker rats were fed identical diets supplemented with linoleic acid or CLA starting at 6 weeks of age. After 8 weeks, the group that received supplemental linoleic acid had developed severe nonalcoholic fatty liver disease, with enlarged livers, and an increase in liver triglycerides that occurs with the disease. Rats who received CLA were largely protected from these effects, and had lower levels of plasma markers of liver injury compared to rats who did not receive CLA. CLA-fed animals also had lower total cholesterol levels, although their plasma triglyceride levels were higher than the rats that were not supplemented with CLA.
When two liver proteins involved in lipid homeostasis were analyzed (CPT and MPT), their activities were found to be greater in the control animals than in rats who received CLA, demonstrating an association with the alleviation of nonalcoholic fatty liver disease. In addition, plasma adiponectin, a substance that improves insulin sensitivity, was increased in CLA-fed rats, and liver tumor necrosis factor-alpha, which is elevated in inflammatory conditions, was suppressed.
In a previous study conducted by the Saga University team, CLA was found to control hyperinsulinemia in Zucker rats. As insulin resistance is the first step in the development of nonalcoholic fatty liver disease, the increase in adiponectin associated with CLA supplementation may be responsible for the protection against the disease observed in this study. Because other studies have found that adiponectin suppresses tumor necrosis factor-alpha, the reduction in this inflammatory cytokine may have prevented the development and progression of nonalcoholic fatty liver disease in rats supplemented with CLA.
Zinc regulates COX-2 expression in animal model of cancer
Researchers from Thomas Jefferson University in Philadelphia have found a reason for the association between esophageal and tongue cancers with a deficiency of zinc. In the January 5 2005 issue of the Journal of the National Cancer Institute, they reported the finding that zinc regulates cyclooxygenase-2 (COX-2), an enzyme that is frequently overexpressed in these and other cancers.
Fifteen rats were fed diets containing sufficient zinc and 90 rats were provided with zinc deficient diets for 5 weeks, at which time the deficient rats showed increased esophageal cell proliferation. Seventy-five of the deficient rats were then administered zinc gluconate and switched to diets sufficient in zinc for 2, 8, 12, 24 or 48 hours after which the esophagus and tongue epithelia were examined. A control group of zinc deficient rats were administered saline.
The esophagus and tongue of the zinc deficient rats exhibited hyperplasia and expression of COX-2 at levels 8 to 12 times higher than rats whose diets contained adequate zinc. Replenishment of zinc restored COX-2 expression to almost normal by 48 hours.
In another group of rats given zinc deficient or sufficient diets for five weeks, deficient rats were divided to receive a dose of the COX-2 inhibitors celecoxib or indomethacin, while the remainder received zinc or a placebo. COX-2 expression was found to be lowered after 8 hours in the rats who received the drugs, but not to the extent of that in the group treated with zinc. Cell proliferation was reduced and apopotosis increased in the groups receiving COX-2 inhibitors or zinc, but rats who received zinc had fewer esophageal hyperplastic lesions.
The authors conclude that treatment with zinc corrects the overexpression of COX-2 caused by a deficiency of the mineral, and that the study “raises the possibility that zinc supplementation may have a role in the prevention of oral and esophageal cancer.”
Carotenoids linked to lower rate of prostate cancer in Chinese men
The dietary carotenoid lycopene, which gives tomatoes and watermelon their red color, has been epidemiologically associated with a lower risk of prostate cancer in men residing in western countries where the nutrient is commonly consumed in tomato sauce, pizza and ketchup. The current study, published in the March 2005 issue of the International Journal of Cancer, examined 404 men in southeast China, where dietary patterns differ from those of western countries and the rate of prostate cancer is low.
Participants consisted of 130 men with prostate cancer and 274 hospital inpatients without cancer. Interviews in which food frequency questionnaires were administered provided data on dietary intake that was analyzed to determine the carotenoid content of fruits and vegetables consumed.
The researchers, from Curtin University of Technology in Perth, Australia, found an inverse association between prostate cancer and intake all of the dietary carotenoids examined, which included lycopene, alpha-carotene, beta-cryptoxanthin, lutein and zeaxanthin. Of the 130 foods participants were queried on, tomatoes, pumpkin, spinach, watermelon and citrus fruits were negatively associated with prostate cancer risk.
Subjects whose reported lycopene intake was in the top one-fourth of participants experienced an 82 percent lower risk of prostate cancer than those whose intake was in the lowest quarter. Lutein and zeaxanthin were associated with an even greater reduction in risk, with those in the top quarter of intake experiencing a risk of prostate cancer that was 100 percent lower than those whose intake was the lowest.
The study also found that the participants consumed a greater amount of total carotenoids than American men. This finding could contribute in part to the explanation of the lower incidence of prostate cancer among the Chinese.
L-carnitine protects brain DNA from age-related damage
A report published in the January 2005 issue of the journal Experimental Neurology revealed that the amino acid L-carnitine helps protect the brain of rats from the DNA damage that occurs with aging.
Dr P. A. R. Juliet of Nagoya University in Japan and colleagues gave 4 month old and 24 month old rats 300 milligrams acetyl-L-carnitine per kilogram body weight for 7, 14 and 21 days following which their brain cortex, hippocampus, striatum, hypothalamus and cerebellum were examined for antioxidant enzyme activity, nucleic acid (DNA and RNA) levels, and DNA damage.
Carnitine levels were lower in all brain regions examined in the 24 month old rats than in the 4 month old animals, although longer supplementation with L-carnitine was reflected in increased brain levels of the amino acid in the older animals, which was not observed in the younger rats. Older rats also had lower brain levels of the antioxidant enzymes superoxide dismutase and glutathione peroxidase, as well as lower DNA and RNA levels in the cortex, hippocampus and striatum, however in older rats who received L-carnitine, the researchers found enhanced levels of antioxidants and nucleic acids that increased with duration of the treatment, which again, were not found to be effected by carnitine in the younger rats.
When DNA damage was assessed, it was found to be higher in the older rat brains than in the younger rats, particularly in the cortex, hippocampus and striatum, and carnitine was shown to provide the greatest protection against damage in these areas. L-carnitine did not significantly reduce brain DNA damage in young rats.
The authors propose that L-carnitine provides its neuroprotective effect by promoting energy production, activating a DNA repairing enzyme and enhancing antioxidant status.