Thursday, August 5, 2010

Chew on this: Six dental myths debunked

Chew on This: Six Dental Myths Debunked


ScienceDaily (Aug. 5, 2010) — Brushing, flossing, and twice-yearly dental check-ups are standard for oral health care, but there are more health benefits to taking care of your pearly whites than most of us know. In a review article, a faculty member at Tufts University School of Dental Medicine (TUSDM) debunks common dental myths and outlines how diet and nutrition affects oral health in children, teenagers, expectant mothers, adults and elders.



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Myth 1: The consequences of poor oral health are restricted to the mouth
Expectant mothers may not know that what they eat affects the tooth development of the fetus. Poor nutrition during pregnancy may make the unborn child more likely to have tooth decay later in life. "Between the ages of 14 weeks to four months, deficiencies in calcium, vitamin D, vitamin A, protein and calories could result in oral defects," says Carole Palmer, EdD, RD, professor at TUSDM and head of the division of nutrition and oral health promotion in the department of public health and community service. Some data also suggest that lack of adequate vitamin B6 or B12 could be a risk factor for cleft lip and cleft palate formation.
In children, tooth decay is the most prevalent disease, about five times more common than childhood asthma. "If a child's mouth hurts due to tooth decay, he/she is less likely to be able to concentrate at school and is more likely to be eating foods that are easier to chew but that are less nutritious. Foods such as donuts and pastries are often lower in nutritional quality and higher in sugar content than more nutritious foods that require chewing, like fruits and vegetables," says Palmer. "Oral complications combined with poor diet can also contribute to cognitive and growth problems and can contribute to obesity."
Myth 2: More sugar means more tooth decay
It isn't the amount of sugar you eat; it is the amount of time that the sugar has contact with the teeth. "Foods such as slowly-dissolving candies and soda are in the mouth for longer periods of time. This increases the amount of time teeth are exposed to the acids formed by oral bacteria from the sugars," says Palmer.
Some research shows that teens obtain about 40 percent of their carbohydrate intake from soft drinks. This constant beverage use increases the risk of tooth decay. Sugar-free carbonated drinks and acidic beverages, such as lemonade, are often considered safer for teeth than sugared beverages but can also contribute to demineralization of tooth enamel if consumed regularly.
Myth 3: Losing baby teeth to tooth decay is okay
It is a common myth that losing baby teeth due to tooth decay is insignificant because baby teeth fall out anyway. Palmer notes that tooth decay in baby teeth can result in damage to the developing crowns of the permanent teeth developing below them. If baby teeth are lost prematurely, the permanent teeth may erupt malpositioned and require orthodontics later on.
Myth 4: Osteoporosis only affects the spine and hips
Osteoporosis may also lead to tooth loss. Teeth are held in the jaw by the face bone, which can also be affected by osteoporosis. "So, the jaw can also suffer the consequences of a diet lacking essential nutrients such as calcium and vitamins D and K," says Palmer.
"The jawbone, gums, lips, and soft and hard palates are constantly replenishing themselves throughout life. A good diet is required to keep the mouth and supporting structures in optimal shape."
Myth 5: Dentures improve a person's diet
If dentures don't fit well, older adults are apt to eat foods that are easy to chew and low in nutritional quality, such as cakes or pastries. "First, denture wearers should make sure that dentures are fitted properly. In the meantime, if they are having difficulty chewing or have mouth discomfort, they can still eat nutritious foods by having cooked vegetables instead of raw, canned fruits instead of raw, and ground beef instead of steak. Also, they should drink plenty of fluids or chew sugar-free gum to prevent dry mouth," says Palmer.
Myth 6: Dental decay is only a young person's problem
In adults and elders, receding gums can result in root decay (decay along the roots of teeth). Commonly used drugs such as antidepressants, diuretics, antihistamines and sedatives increase the risk of tooth decay by reducing saliva production. "Lack of saliva means that the mouth is cleansed more slowly. This increases the risk of oral problems," says Palmer. "In this case, drinking water frequently can help cleanse the mouth."
Adults and elders are more likely to have chronic health conditions, like diabetes, which are risk factors for periodontal disease (which begins with an inflammation of the gums and can lead to tooth loss). "Type 2 diabetes patients have twice the risk of developing periodontal disease of people without diabetes. Furthermore, periodontal disease exacerbates diabetes mellitus, so meticulous oral hygiene can help improve diabetes control," says Palmer.
This article appears in the July/August issue of Nutrition Today.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Tufts University, Health Sciences.




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Palmer et al. It's More Than Just Candy : Important Relationships Between Nutrition and Oral Health. Nutrition Today, 2010; 45 (4): 154 DOI: 10.1097/NT.0b013e3181e98969





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Pancreatic cancers use fructose, common in the Western diet, to fuel their growth

Pancreatic Cancers Use Fructose, Common in the Western Diet, to Fuel Their Growth


ScienceDaily (Aug. 2, 2010) — Pancreatic cancers use the sugar fructose, very common in the Western diet, to activate a key cellular pathway that drives cell division, helping the cancer to grow more quickly, a study by researchers at UCLA's Jonsson Comprehensive Cancer Center has found.



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Although it's widely known that cancers use glucose, a simple sugar, to fuel their growth, this is the first time a link has been shown between fructose and cancer proliferation, said Dr. Anthony Heaney, an associate professor of medicine and neurosurgery, a Jonsson Cancer Center researcher and senior author of the study.
"The bottom line is the modern diet contains a lot of refined sugar including fructose and it's a hidden danger implicated in a lot of modern diseases, such as obesity, diabetes and fatty liver," said Heaney, who also serves as director of the Pituitary Tumor and Neuroendocrine Program at UCLA. "In this study, we show that cancers can use fructose just as readily as glucose to fuel their growth."
The study appeared in the Aug. 1 issue of the peer-reviewed journal Cancer Research.
Sources of fructose in the Western diet include cane sugar (sucrose) and high fructose corn syrup (HFCS), a corn-based sweetener that has been on the market since about 1970. HFCS accounts for more than 40 percent of the caloric sweeteners added to foods and beverages, and it is the sole sweetener used in American soft drinks.
Between 1970 and 1990, the consumption of HFCS in the U.S. has increased over 1,000 percent, according to an article in the April 2004 issue of the American Journal of Clinical Nutrition. Food companies use HFCS -- a mixture of fructose and glucose -- because it's inexpensive, easy to transport and keeps foods moist. And because it is so sweet, it's cost effective for companies to use small quantities of HCFS in place of more expensive sweeteners or flavorings.
In his study, Heaney and his team took pancreatic tumors from patients and cultured and grew the malignant cells in petri dishes. They then added glucose to one set of cells and fructose to another. Using mass spectrometry, they were able to follow the carbon-labeled sugars in the cells to determine what exactly they were being used for and how.
Heaney found that the pancreatic cancer cells could easily distinguish between glucose and fructose even though they are very similar structurally, and contrary to conventional wisdom, the cancer cells metabolized the sugars in very different ways. In the case of fructose, the pancreatic cancer cells used the sugar in the transketolase-driven non-oxidative pentose phosphate pathway to generate nucleic acids, the building blocks of RNA and DNA, which the cancer cells need to divide and proliferate.
"Traditionally, glucose and fructose have been considered as interchangeable monosaccharide substrates that are similarly metabolized, and little attention has been given to sugars other than glucose," the study states. "However, fructose intake has increased dramatically in recent decades and cellular uptake of glucose and fructose uses distinct transporters ... these findings show that cancer cells can readily metabolize fructose to increase proliferation. They have major significance for cancer patients, given dietary refined fructose consumption."
As in anti-smoking campaigns, a federal effort should be launched to reduce refined fructose intake, Heaney said.
"I think this paper has a lot of public health implications," Heaney said. "Hopefully, at the federal level there will be some effort to step back on the amount of HFCS in our diets."
Heaney said that while this study was done in pancreatic cancer, these finding may not be unique to that cancer type.
Going forward, Heaney and his team are exploring whether it's possible to block the uptake of fructose in the cancer cells with a small molecule, taking away one of the fuels they need to grow. The work is being done in cell lines and in mice, Heaney said.
The study was funded by the National Institutes of Health, the Hirschberg Foundation and the Jonsson Cancer Center.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of California - Los Angeles, via EurekAlert!, a service of AAAS.




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Haibo Liu, Danshan Huang, David L. Mcarthur, Laszlo G. Boros, Nicholas Nissen, and Anthony P. Heaney. Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth. Cancer Research, August 1, 2010 70:6368-6376; Published OnlineFirst July 20, 2010 DOI: 10.1158/0008-5472.CAN-09-4615





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One high-fat diet, two different outcomes: The path to obesity becomes clearer

One High-Fat Diet, Two Different Outcomes: The Path to Obesity Becomes Clearer


ScienceDaily (Aug. 5, 2010) — Why is it that two people can consume the same high fat, high-calorie Western diet and one becomes obese and prone to diabetes while the other maintains a slim frame? This question has long baffled scientists, but a study by Yale School of Medicine researchers provides a simple explanation: weight is set before birth in the developing brain.



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The results are reported online the week of August 2 in the Proceedings of the National Academy of Sciences.
Led by Tamas Horvath, chair and professor of comparative medicine and professor of neurobiology and obstetrics & gynecology at Yale School of Medicine, the research team analyzed the same question in specific groups of rats. These animals have been bred so that their vulnerability to diet-induced obesity is known before they would be put on high-fat, high-calorie diet diets.
Horvath said animals that become obese already had a significant difference in the feeding center of the brain. Neurons that are supposed to signal when you've eaten enough and when to burn calories, are much more sluggish in these animals because they are inhibited by other cells. In animals resistant to obesity, these satiety signaling neurons are much more active and ready to signal to the rest of the brain and peripheral tissues when enough food has been consumed.
"It appears that this base wiring of the brain is a determinant of one's vulnerability to develop obesity," said Horvath, who is also co-director of the Yale Program in Integrative Cell Signaling and Neurobiology of Metabolism. "These observations add to the argument that it is less about personal will that makes a difference in becoming obese, and, it is more related to the connections that emerge in our brain during development."
Horvath points to other unwanted consequences of these brain mechanisms. "Those who are vulnerable to diet-induced obesity also develop a brain inflammation, while those who are resistant, do not," he said. "This emerging inflammatory response in the brain may also explain why those who once developed obesity have a harder time losing weight."
Diet-induced obesity has become one of the most critical medical problems in the United States. In particular, the incidence of childhood obesity has reached unprecedented levels. Since genetics alone cannot explain the surge of obesity in society, investigators have been trying to determine the primary underpinnings of the vulnerability to develop obesity on a Western diet.
"What genetic, epigenetic and environmental factor determines this base wiring in the brain is a very important issue to address," said Horvath. "Specifically, the emerging view is that besides genetics, maternal impact on the developing brain is likely to be critical to imprint these feeding circuits thereby determining one's vulnerability or resistance to obesity."
The study was supported by the National Institutes of Health and the American Diabetes Association.
Other Yale authors include Beatrix Sarman, Peter Sotonyi, Marya Shanabrough, Erzsebet Borok and Sabrina Diano. The study also included authors from the following institutions: Monash University, University of Cincinnati, German Institute of Human Nutrition Potsdam-Rehbrücke, Department of Veterans Affairs New Jersey Health Care System and University of Medicine and Dentistry New Jersey.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Yale University.




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Tamas L. Horvath, Beatrix Sarman, Cristina García-Cáceres, Pablo J. Enriori, Peter Sotonyi, Marya Shanabrough, Erzsebet Borok, Jesus Argente, Julie A. Chowen, Diego Perez-Tilve, Paul T. Pfluger, Hella S. Brönneke, Barry E. Levin, Sabrina Diano, Michael A. Cowley, and Matthias H. Tschöp. Synaptic input organization of the melanocortin system predicts diet-induced hypothalamic reactive gliosis and obesity. PNAS, August 2, 2010 DOI: 10.1073/pnas.1004282107





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Tuesday, August 3, 2010

Adolescents with type 2 diabetes have diminished cognitive performance and brain abnormalities, study finds

Adolescents With Type 2 Diabetes Have Diminished Cognitive Performance and Brain Abnormalities, Study Finds


ScienceDaily (Aug. 2, 2010) — A study by researchers at NYU Langone Medical Center have found that obese adolescents with type 2 diabetes have diminished cognitive performance and subtle abnormalities in the brain as detected by Magnetic Resonance Imaging (MRI). Identification of cognitive impairments as a complication of type 2 diabetes emphasizes the importance of addressing issues of inactivity and obesity, two important risk factors for the development of the disease among the young.



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The study appeared online in the journal Diabetologia, July 30, 2010.
"This is the first study that shows that children with type 2 diabetes have more cognitive dysfunction and brain abnormalities than equally obese children who did not yet have marked metabolic dysregulation from their obesity, " says Antonio Convit, MD, professor of Psychiatry and Medicine at NYU Langone Medical Center and the Nathan S. Kline Institute for Psychiatric Research. "The findings are significant because they indicate that insulin resistance from obesity is lowering children's cognitive performance, which may be affecting their ability to perform well in school."
Researchers studied 18 obese adolescents with type 2 diabetes and compared them to equally obese adolescents from the same socioeconomic and ethnic background but without evidence of marked insulin resistance or pre-diabetes. Investigators found that adolescents with type 2 diabetes not only had significant reductions in performance on tests that measure overall intellectual functioning, memory, and spelling, which could affect their school performance, but also had clear abnormalities in the integrity of the white matter in their brains.
"We have previously found brain abnormalities in adults with Type 2 diabetes, but believed those changes might have been a result of vascular disease," adds Dr. Convit. "Now we see that subtle changes in white matter of the brain in adolescents may be a result of the abnormal physiology that accompanies type 2 diabetes. If we can improve insulin sensitivity and help children through exercise and weight loss, perhaps we can reverse these deficits."
Co-authors of the study include P.L. Yau, W.H. Tsui, B.A. Ardekani of NYU Langone Medical Center and the Nathan S. Klein Institute for Psychiatric Research.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by NYU Langone Medical Center / New York University School of Medicine.




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P. L. Yau, D. C. Javier, C. M. Ryan, W. H. Tsui, B. A. Ardekani, S. Ten and A. Convit. Preliminary evidence for brain complications in obese adolescents with type 2 diabetes mellitus. Diabetologia, 2010; DOI: 10.1007/s00125-010-1857-y





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Exercise and caloric restriction rejuvenate synapses in lab mice

Exercise and Caloric Restriction Rejuvenate Synapses in Lab Mice


ScienceDaily (Aug. 2, 2010) — Harvard University researchers have uncovered a mechanism through which caloric restriction and exercise delay some of the debilitating effects of aging by rejuvenating connections between nerves and the muscles that they control.



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The research, conducted in the labs of Joshua Sanes and Jeff Lichtman and described this week in the journal Proceedings of the National Academy of Sciences, begins to explain prior findings that exercise and restricted-calorie diets help to stave off the mental and physical degeneration of aging.
"Caloric restriction and exercise have numerous, dramatic effects on our mental acuity and motor ability," says Sanes, a professor of molecular and cellular biology and director of the Center for Brain Science at Harvard. "This research gives us a hint that the way these extremely powerful lifestyle factors act is by attenuating or reversing the decline in our synapses."
Sanes says their research, conducted with mice genetically engineered so their nerve cells glow in fluorescent colors, shows some of the debilitation of aging is caused by deterioration of connections that nerves make with the muscles they control, structures called neuromuscular junctions. These microscopic links are remarkably similar to the synapses that connect neurons to form information-processing circuits in the brain.
In a healthy neuromuscular synapse, nerve endings and their receptors on muscle fibers are almost a perfect match, like two hands placed together, finger to finger, palm to palm. This lineup ensures maximum efficiency in transmitting the nerve's signal from the brain to the muscle, which is what makes it contract during movement.
As people age, however, the neuromuscular synapses can deteriorate in several ways. Nerves can shrink, failing to cover the muscle's receptors completely. The resulting interference with transmission of nerve impulses to the muscles can result in wasting and eventually even death of muscle fibers. This muscle wasting, called sarcopenia, is a common and significant clinical problem in the elderly.
The new work showed that mice on a restricted-calorie diet largely avoid that age-related deterioration of their neuromuscular junctions, while those on a one-month exercise regimen when already elderly partially reverse the damage.
"With calorie restriction, we saw reversal of all aspects of the synapse disassembly. With exercise, we saw a reversal of most, but not all," Sanes says.
Because of the study's structure -- mice were on calorie-restricted diets for their whole lives, while those that exercised did so for just a month late in life -- Sanes cautions against drawing conclusions about the effectiveness of exercise versus calorie restriction. He notes that longer periods of exercise might have more profound effects, a possibility he and Lichtman are now testing.
Though much of Sanes and Lichtman's work focuses on brain synapses, both have investigated neuromuscular synapses for many years. Neuromuscular junctions are large enough to be viewed by light microscopy, and can be a jumping-off point for brain study, highlighting areas of inquiry and potential techniques.
"These findings in neuromuscular synapses make us curious to know whether similar effects might occur in brain synapses," Sanes says.
While the changes to the synapses through caloric restriction and exercise were clear in the images the researchers obtained, Sanes cautioned that their work was structural, not functional, and they have not yet tested how well the synapses worked.
The research, largely conducted by postdoctoral researchers Gregorio Valdez, Juan Tapia, and Hyuno Kang, was funded by the National Institute on Aging, National Institute of Neurological Disorders and Stroke, and Ellison Medical Foundation.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Harvard University. The original article was written by Alvin Powell.




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Gregorio Valdez, Juan C. Tapia, Hyuno Kang, Gregory D. Clemenson, Jr., F. H. Gage, Jeff W. Lichtman, and Joshua R. Sanes. Attenuation of age-related changes in mouse neuromuscular synapses by caloric restriction and exercise. PNAS, August 2, 2010 DOI: 10.1073/pnas.1002220107





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Monday, August 2, 2010

Nutritional labeling and point-of-purchase signs influence healthy food choices

Nutritional Labeling and Point-of-Purchase Signs Influence Healthy Food Choices


ScienceDaily (Aug. 2, 2010) — Poor diet and physical inactivity leading to obesity are poised to overtake tobacco use as the leading cause of preventable death in the United States. With over 30% of U.S. adults obese, the significant adverse health effects of obesity (including heart disease and diabetes) are widespread throughout the country. Two studies published in the August issue of the Journal of the American Dietetic Association shed light on behaviors regarding food choices and good nutrition and report on how nutritional labeling and point-of-purchase signs are influencing healthy food choices.



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"Food Label Use and Its Relation to Dietary Intake among U.S. Adults" by Nicholas J. Ollberding, PhD, Randi L. Wolf, PhD, and Isobel Contento, PhD, all of the Program in Nutrition, Department of Health and Behavior Studies, Teachers College, Columbia University, examined to what extent people used the nutritional label on food products and whether that use affected their nutrient intake.
Using a nationally representative sample of U.S. adults who participated in the 2005-2006 National Health and Nutrition Examination Survey (NHANES), the authors found that 61.6% of participants reported using the nutrition facts panel, 51.6% used the list of ingredients, 47.2% read the serving size, and 43.8% reviewed health claims at least sometimes when deciding to purchase a food product.
Significant differences in mean nutrient intake of total calories, total fat, saturated fat, cholesterol, sodium, dietary fiber, and sugars were observed between food label users and non-users with label users reporting healthier nutrient consumption. The greatest differences observed were for total calories and fat and for use of specific nutrient information on the food label.
"If the food label is to have a greater public health impact, rates of use will likely need to be increased among U.S. adults," commented Professor Ollberding. "Low rates of label use also suggest that national campaigns or modification of the food label may be needed to reduce the proportion of the population not using this information. Possible changes to the current label that have been suggested include bolding calorie information, reporting the total nutrient intake for foods likely to be consumed in a single sitting, and using more intuitive labeling that requires less cognitive processing such as a red, yellow, and green 'traffic light' signs on the front of the label. The food label alone is not expected to be sufficient in modifying behavior ultimately leading to improved health outcomes, but may be used by individuals and nutrition professionals as a valuable and motivating tool in our efforts to combat obesity and diet-related chronic disease."
A pilot study of a Point-of-Purchase (POP) program was shown to influence the purchasing behaviors of a multi-ethnic college population shopping at an on-campus convenience store. The results are reported in "Point-of-Purchase Nutrition Information Influences Food-Purchasing Behaviors of College Students: A Pilot Study" by Marjorie R. Freedman, PhD, and Rachel A. Connors, MS, from the Department of Nutrition, Food Science & Packaging, San Jose State University.
This 11-week study collected baseline sales data for 6 weeks during the middle of the Fall 2008 semester. After students returned from Winter break, "Eat Smart" program materials featuring the "Fuel Your Life" logo were placed in the on-campus convenience store. Sales data were collected during the middle of the Spring 2009 semester for 5 weeks, ending just before students left for Spring break.
Healthful items in seven food categories (cereal, bread, soup, cracker, canned vegetable, granola/energy bar, and salad dressing) were tagged throughout the market. There was no difference in price between the tagged and untagged items. While no significant difference in sales of any particular food item was observed between baseline and intervention, overall sales of tagged items, as a percentage of total sales in the cereal, soup, and cracker categories, increased as a result of the intervention, while sales of tagged bread items decreased. Though not statistically significant, the intervention resulted in a 3.6% increase in the percentage of sales from tagged items.
Writing in the article, Freedman and Connor state, "This pilot project was the first to use computerized sales data to examine the effect of a POP nutrition information program on the food-buying habits of multi-ethnic college students. Promising (albeit, not statistically significant) results imply that students were influenced by "Fuel Your Life" shelf tags and related materials. Despite several study limitations, the program was successful in increasing the percentage of tagged food items sold relative to other non-tagged items in the same category. Keeping all items in the same category at the same price meant that consumer choice was based on perceived nutritional benefit, not economics."
"This research indicates that a simple logo helped students identify healthful food choices, and positively influenced food choice," commented Professor Freedman. "It would be interesting to determine if a combination of point-of-purchase nutrition information, coupled with economic incentives (e.g. lower prices for healthier foods) would further drive consumers to choose these healthier food items. We must aggressively test such options in light of the increasing threat of obesity to the health of our society."
Both studies appear in the Journal of the American Dietetic Association, Volume 110, Issue 8 (August 2010) published by Elsevier.

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Ollberding NJ, Wolf RL, Contento I. Food label use and its relation to dietary intake among U.S. adults. J Am Diet Assoc, 2010; 110: 1233-1237 DOI: 10.1016/j.jada.2010.05.007
Freedman MR, Connors RA. Point-of-purchase nutrition information influences food-purchasing behaviors of college students: A pilot study. J Am Diet Assoc, 2010;110:1222-1226 DOI: 10.1016/j.jada.2010.05.002





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Certain meat components may increase bladder cancer risk, study suggests

Certain Meat Components May Increase Bladder Cancer Risk, Study Suggests


ScienceDaily (Aug. 2, 2010) — A new study suggests that consuming specific compounds in meat related to processing methods may be associated with an increased risk of developing bladder cancer. Published early online in Cancer, a peer-reviewed journal of the American Cancer Society, the findings may be relevant for understanding the role of dietary exposures in cancer risk.



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Eating red and processed meats has been linked to an increased risk of developing several different types of cancer. Animal studies have identified a number of compounds in meat that might account for this association. These include heterocyclic amines, polycyclic aromatic hydrocarbons, and N-nitroso compounds. Nitrate and nitrite are added to processed meats and are known precursors to N-nitroso compounds.
Amanda J. Cross, PhD, of the National Cancer Institute in Rockville and colleagues conducted one of the first prospective studies -- the NIH-AARP Diet and Health Study -- to assess the relationship between intake of these meat-related compounds and the risk of developing bladder cancer. They used information gathered through questionnaires to assess the types of meat consumed as well as how meat was prepared and cooked to estimate the intake of these meat-related compounds.
The investigators had information from approximately 300,000 men and women aged 50 to 71 years from eight US states. At the start of the study (1995 to 1996), all participants completed lifestyle and dietary questionnaires about their usual consumption of foods and drinks. The participants were followed for up to eight years, during which time 854 people were diagnosed with bladder cancer.
People whose diets had the highest amount of total dietary nitrite (from all sources and not just from meat), as well as those whose diets had the highest amount of nitrate plus nitrite from processed meats had a 28 percent to 29 percent increased risk of developing bladder cancer compared with those who consumed the lowest amount of these compounds. This association between nitrate/nitrite consumption and bladder cancer risk may explain why other studies have observed an association between processed meats and increased bladder cancer risk.
"Our findings highlight the importance of studying meat-related compounds to better understand the association between meat and cancer risk," said Dr. Cross. "Comprehensive epidemiologic data on meat-related exposures and bladder cancer are lacking; our findings should be followed up in other prospective studies," she added.

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The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Cancer Society, via EurekAlert!, a service of AAAS.




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Leah M. Ferrucci, Rashmi Sinha, Mary H. Ward, Barry I. Graubard, Albert R. Hollenbeck, Briseis A. Kilfoy, Arthur Schatzkin, Dominique S. Michaud, and Amanda J. Cross. Meat and components of meat and the risk of bladder cancer in the NIH-AARP Diet and Health Study. Cancer, 2010; DOI: 10.1002/cncr.25463





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