Research - Diet
Red Meat Intake and Risk of ESRD
- Quan-Lan Jasmine Lew*,
- Tazeen Hasan Jafar†‡,
- Hiromi Wai Ling Koh§,
- Aizhen Jin‖,
- Khuan Yew Chow‖,
- Jian-Min Yuan¶** and
- Woon-Puay Koh†§
Randomized controlled trials suggest that protein restriction may retard the progression of CKD toward ESRD. However, the effects of dietary protein intake level and the food sources of dietary protein on the risk of ESRD in the general population remain unclear. We investigated these effects in the Singapore Chinese Health Study, a prospective population-based cohort that recruited 63,257 Chinese adults aged 45–74 years from 1993 to 1998. We collected habitual diet information via a validated semiquantitative food frequency questionnaire and identified ESRD via record linkage with a nationwide registry. In all, 951 cases of ESRD occurred over a mean follow-up of 15.5 years. Regarding total protein intake, compared with the lowest quartile, the three higher quartiles combined had a hazard ratio for ESRD of 1.24 (95% confidence interval [95% CI], 1.05 to 1.46), but the dose-dependent association across the quartiles was not statistically significant (Ptrend=0.16). Red meat intake strongly associated with ESRD risk in a dose-dependent manner (hazard ratio for highest quartile versus lowest quartile,1.40 [95% CI, 1.15 to 1.71;Ptrend<0.001]). Intake of poultry, fish, eggs, or dairy products did not associate with risk of ESRD. In substitution analysis, replacing one serving of red meat with other food sources of protein associated with a maximum relative risk reduction of 62.4% (95% CI, 33.1 to 78.9; P<0.01). Our study shows that red meat intake may increase the risk of ESRD in the general population and substituting alternative sources of protein may reduce the incidence of ESRD.
Source : J Am Soc Nephrol.
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Plasma acylcarnitines and risk of cardiovascular disease: effect of Mediterranean diet interventions
- Marta Guasch-Ferré4,6,7,
- Yan Zheng4,
- Miguel Ruiz-Canela7,8,
- Adela Hruby4,
- Miguel A Martínez-González7,8,
- Clary B Clish9,
- Dolores Corella7,10,
- Ramon Estruch7,11,
- Emilio Ros7,12,
- Montserrat Fitó7,13,
- Courtney Dennis9,
- Isabel M Morales-Gil14,
- Fernando Arós15,
- Miquel Fiol16,
- José Lapetra7,17,
- Lluís Serra-Majem7,18,
- Frank B Hu4,5,19, and
- Jordi Salas-Salvadó6,7
Background: Previous studies have suggested that metabolite profiles of elevated acylcarnitines were associated with increased risk of cardiovascular disease (CVD) in populations with established coronary disease. However, to our knowledge, this association has not been evaluated in the context of primary cardiovascular prevention.
Objectives: We evaluated the association between 28 plasma acylcarnitine species and risk of incident CVD and the potential modifying effect of Mediterranean diet (MedDiet) interventions.
Design: We measured plasma acylcarnitines with the use of high-throughput liquid chromatography–tandem mass spectrometry at baseline and after 1 y of follow-up, both individually and classified into short-, medium-, or long-chain scores, in a case-cohort study within the Prevención con Dieta Mediterránea (PREDIMED) study, which is a randomized Mediterranean dietary intervention for primary cardiovascular prevention. A randomly selected subcohort (n = 751) and all available incident CVD cases (n = 229) after 4.8 y of follow-up were included in the current study.
Results: After adjustment for age, sex, body mass index, and other CVD risk factors, participants in the highest quartile of baseline short- and medium-chain acylcarnitines had a higher risk of CVD than did participants in the lowest quartile [HRs: 1.80 (95% CI: 1.11, 2.91; P-trend 0.01) and 1.55 (95% CI: 1.01, 2.48; P-trend = 0.04), respectively]. Increased short-chain acylcarnitines after 1 y were associated with higher risks of total CVD and stroke. Participants with higher baseline concentrations of short-, medium-, and long-chain acylcarnitines who were randomly assigned to the control group had a higher risk of CVD than did subjects with lower concentrations of acylcarnitines who were assigned to the MedDiet group.
Conclusions: Our data support the conclusion that metabolite profiles characterized by elevated concentrations of acylcarnitines are independently associated with risks of total CVD and stroke alone in participants at high risk of CVD. MedDiet interventions may mitigate the adverse associations shown between higher concentrations of acylcarnitines and CVD.
Source : American Journal of Clinical Nutrition
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Low Fat Diet Helps Postmenopausal Women Avoid Deadly Breast Cancer
A large randomized clinical trial found that postmenopausal women who stayed on a low fat diet for 8 years had a reduced risk of death from invasive breast cancers and improved survival rates compared with women who did not follow the dietary regimen.1 The study was presented at a clinical trial plenary session at the American Association for Cancer Research Annual Meeting, held April 16-20, 2016 in New Orleans, Louisiana.
This analysis used data from 48,835 postmenopausal women who participated in the randomized, controlled, dietary modification trial that was part of the Women's Health Initiative. Though an association between dietary fat intake and breast cancer has been observed for about half a century, this study sought to clarify the effects of a low-fat dietary pattern on breast cancer.
The participating women were age 50 to 79 years, had no prior breast cancer, normal mammograms, and normal dietary fat intake. Of those, 19,541 women were put on a low-fat diet with nutritionist-led group sessions that sought to reduce fat intake reduction to 20% of energy and increase the consumption of fruits, vegetables, and grain. The other 29,294 women in the trial followed their usual dietary patterns.
After about 8 years of remaining on the low fat diet, 1,767 of the women were diagnosed with breast cancer. Researchers found the breast cancer overall survival from diagnosis was higher in the dietary group: 82% versus 78%. The researchers said this reduction is due, in part, to better survival following breast cancer diagnosis.
"This was the first time we had examined the deaths after breast cancer among this group, and we found that a sustained low-fat diet increased the survival rates among postmenopausal women after a breast cancer diagnosis," said presenting author Rowan Chlebowski, MD, PhD, of the Los Angeles Biomedical Research Institute in California. "The study also suggests that women would need to remain on the low fat diets to maintain the benefits of the dietary intervention."
The 2 groups of women had similar breast cancer characteristics, including size, nodal status, and distribution of poor prognosis, triple-negative cancers and HER2-positive cancers. However, the dietary group had fewer progesterone-receptor-negative cancers (28.4% versus 33%). In addition, researchers noted lower cardiovascular disease mortality in the dietary group.
1. Chlebowski RT, Aragaki AK, Anderson GL, et al. Low-fat dietary pattern and breast cancer mortality in the Women's Health Initiative (WHI) randomized trial. Abstract CT043. Presented at American Association for Cancer Research Annual Meeting, held April 16-20, 2016 in New Orleans, Louisiana.
Source : Oncology Nurse Advisor
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Sugar and Cancer: Mitigating the Affects of Diet on Cancer
Food speaks to our genes; its message or signal can turn the immune system on or off. Consumption of a high carbohydrate or sugar diet can increase risk of cancer. The affect of diet on cancer risk and prevention were explained in an oral presentation at the 2nd AnnualOncology Nurse Advisor Navigation Summit.1
Epigenetics is the variations caused by external modifications to DNA such as environment, exercise, stress, meditation, spirituality, and diet, explained Sharon Meyer, DiplON, CNC, of Integrative Nutrition. Sugar or glucose feeds cancer, although not directly. Insulin chaperones sugar or glucose into the cells. Insulin docks onto an insulin receptor on the cell surface enabling sugar/glucose to enter the cell, where the mitochondria convert it into energy. Too much sugar increases blood sugar and insulin levels. Over time, healthy cells are no longer able to receive sugar. Insulin receptors become sensitive to insulin and no longer respond; this is insulin resistance.
Cancer cells are poor energy metabolizers. Their surfaces are covered with insulin receptors that continually chaperone glucose into the cancer cells. Therefore, even when healthy cells become insulin resistant, cancer cells continue to accept and metabolize sugar. Insulin releases glucose into the cancer cells, it goes through the nucleus causing an epigenetic effect of turning on genes that prompt cell division. Meyer described this effect as “Like a foot on a gas pedal, stimulating cancer growth.”
“If the foods you ate could turn off the expression of your cancer genes, and turn on tumor suppressor genes, what would you have for dinner?” asked Meyer. Her answer: Vegetables. A lot of them and a variety of them. “Eat from the rainbow,” advised Meyer.
Vegetables are high in phytochemicals, which protect plants from the environment, stressors, sun, toxins, and more; humans need phytochemicals to be healthy. They are major communicators to our genes. They support detoxification, boost immunity, improve heart health, promote healthy estrogen metabolism, stimulate apoptosis, reduce inflammation, and feed the gut bugs (microbiome).
Other components of a healthy diet include fats and oils and protein. Healthy choices for fats and oils include foods such as avocadoes, fish (eg, sardines, herring, salmon), nuts and seeds, nut butters, butter, and ghee. Extra virgin olive oil, flaxseed oil, coconut oil/butter/milk, nut oils (eg, walnut, hazelnut, macadamia), and avocado oils are better choices.
Protein sources include eggs, fish, poultry, beef, lamb, and lean pork. Whole-milk dairy and whey protein are other recommendations. Animal protein should be free-range, pasture raised, or organic, and wild fish.
In closing, Meyer's advice for patients with cancer is to eat appealing foods when they can, and not to stress over their diet. “Plenty of time to clean up later!”
1. Meyer S. Nutrition & Cancer. Oral presentation at: Oncology Nurse Advisor Navigation Summit; April 7-9, 2016; Orlando, FL.
Source : Oncology Nurse Advisor
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Gluten exacerbates IgA nephropathy in humanized mice through gliadin–CD89 interaction
Christina Papista1,2,3,4, Sebastian Lechner1,2,3,4, Sanae Ben Mkaddem1,2,3,4, Marie-Bénédicte LeStang1,2,3,4, Lilia Abbad1,2,3,4, Julie Bex-Coudrat1,2,3,4, Evangéline Pillebout5, Jonathan M Chemouny1,2,3,4, Mathieu Jablonski6, Martin Flamant1,2,4,7, Eric Daugas1,2,3,4,6, François Vrtovsnik1,2,3,4,6, Minas Yiangou8, Laureline Berthelot1,2,3,4,10 and Renato C Monteiro1,2,3,4,9,10
IgA1 complexes containing deglycosylated IgA1, IgG autoantibodies, and a soluble form of the IgA receptor (sCD89), are hallmarks of IgA nephropathy (IgAN). Food antigens, notably gluten, are associated with increased mucosal response and IgAN onset, but their implication in the pathology remains unknown. Here, an IgAN mouse model expressing human IgA1 and CD89 was used to examine the role of gluten in IgAN. Mice were given a gluten-free diet for three generations to produce gluten sensitivity, and then challenged for 30 days with a gluten diet. A gluten-free diet resulted in a decrease of mesangial IgA1 deposits, transferrin 1 receptor, and transglutaminase 2 expression, as well as hematuria. Mice on a gluten-free diet lacked IgA1-sCD89 complexes in serum and kidney eluates. Disease severity depended on gluten and CD89, as shown by reappearance of IgAN features in mice on a gluten diet and by direct binding of the gluten-subcomponent gliadin to sCD89. A gluten diet exacerbated intestinal IgA1 secretion, inflammation, and villous atrophy, and increased serum IgA1 anti-gliadin antibodies, which correlated with proteinuria in mice and patients. Moreover, early treatment of humanized mice with a gluten-free diet prevented mesangial IgA1 deposits and hematuria. Thus, gliadin–CD89 interaction may aggravate IgAN development through induction of IgA1–sCD89 complex formation and a mucosal immune response. Hence, early-stage treatment with a gluten-free diet could be beneficial to prevent disease.
Source : Journal Kidney International
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Saturated high-fat feeding can cause impairments in critical motivation brain pathway
High-fat feeding can cause impairments in the functioning of the mesolimbic dopamine system, says Stephanie Fulton of the University of Montreal and the CHUM Research Centre (CRCHUM.) This system is a critical brain pathway controlling motivation. Fulton’s findings, published today in Neuropsychopharmacology, may have great health implications. “Our research shows that independent of weight gain and obesity, high-fat feeding can cause impairments in the functioning of the brain circuitry profoundly implicated in mood disorders, drug addiction, and overeating – several states and pathologies that impinge on motivation and hedonia,” Fulton explained. Hedonia relates to a mental state of wellbeing. “Another key finding is that the effects of prolonged high-fat feeding to dampen the sensitivity of this brain reward system are specific to saturated fats – palm oil used in this study – but not monounsaturated fat such as the olive oil used in this study.”
The research team obtained these findings by working with three groups of rats. The first group of rats was the control group: they were given a low-fat diet containing roughly equal amounts of monounsaturated and saturated fatty acids. The second group was given a monounsaturated high fat diet, of which 50% of the calories were from fat derived from olive oil. The third group was given a saturated high fat diet – again, 50% of the calories were from fat, but this time derived from palm oil. The high-fat diets were all the same in terms of sugars, proteins, fat content and caloric density, and the animals were free to eat as much or as little as they liked. After eight weeks, all of the rats still had comparable body weights and levels of insulin, leptin (which are major metabolic hormones) and relative glycemia.
At this time, the rats underwent a series of behavioural and biochemical tests known to be indicative of the functioning of rats’ dopamine system. “We established that the rats on the palm diet had a significantly blunted dopamine function,” said Cecile Hryhorczuk, the first author of the study. “Our research group and others hypothesize that this leads the brain to try to compensate by heightening reward-seeking behaviour, much like the phenomenon of drug tolerance where one has to increase the drug dose over time to get the same high. So, a person consuming too much saturated fat may then compensate a reduced reward experience by seeking out and consuming more high-fat and high-sugar foods to get the same level of pleasure or reward.”
Fulton’s study is the first of its kind to show that, regardless of weight changes, unrestrained intake of saturated fats can have negative effects on the controls of motivation by the brain. “As we were able to control for changes in body weight, hormones and glucose levels, we think that the fats may be affecting the dopamine system by a direct action in the brain,” Fulton said. “We in fact have separate evidence that brain inflammation could be involved in this process, as it is evoked by saturated high-fat feeding, which will be presented in a future publication.”
About this study:
Stephanie Fulton and her colleagues published “Dampened mesolimbic dopamine function and signaling by saturated but not monounsaturated dietary lipids” in Neuropsychopharmacology on July 14, 2015. Stephanie Fulton, PhD, is a professor at the University of Montreal’s Department of Nutrit
Source : Newswise
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Egg consumption is associated with increased risk of ovarian cancer: Evidence from a meta-analysis of observational studies
Sai-tian Zeng , Liang Guo, Shi-kai Liu, Dong-hui Wang, Jie Xi, Ping Huang, Dan-tong Liu, Jie-fan Gao, Jing Feng,Liang Zhang
The findings of epidemiologic studies on the association between egg consumption and ovarian cancer risk remain conflicting. The aim of this meta-analysis was to investigate whether an association exists between egg intake and ovarian cancer risk in epidemiologic studies.
A literature search was carried out using PUBMED, EMBASE, and Cochrane Library Central database for all medical literature published in English-language journals up to August 2013. Before meta-analysis, between-study heterogeneity and publication bias were assessed using adequate statistical tests. Fixed-effect and random-effect models were used to estimate summary relative risks (RR) and the corresponding 95% confidence intervals (CIs). Subgroup analyses and sensitivity analysis were also performed.
A total of 12 eligible studies (six case-control studies and six cohort studies) were included, involving 629,453 subjects and 3728 ovarian cancer cases. We found that high egg intake (comparing the highest with the lowest category) was associated with a significant increased risk of ovarian cancer (RR = 1.21, 95% CI [1.06, 1.38]). When we examined whether the associations differed by study type, statistically significant effect of egg intake on ovarian cancer was observed among case-control studies (RR = 1.22, 95% CI [1.03, 1.43]), but not among cohort studies (RR = 1.20, 95% CI [0.97, 1.48]).
Our findings suggest that egg consumption may increase ovarian cancer risk. Additional studies, especially large prospective cohort studies, are warranted to confirm the findings.
Source : clinical Nutrition
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C-reactive protein response to a vegan lifestyle intervention
Jay T. Sutliffe, , Lori D. Wilson, , Hendrik D. de Heer, , Ray L. Foster, , Mary Jo Carnot
- •Most participants had a drop in their CRP level.
- •The vegan diet significantly reduced systemic inflammation.
- •Amount of exercise was not significantly predictive of changes in CRP.
- •Length of stay was not significantly predictive of changes in CRP.
This brief lifestyle intervention, including a vegan diet rich in fresh fruits and vegetables, whole grains and various legumes, nuts and seeds, significantly improved health risk factors and reduced systemic inflammation as measured by circulating CRP. The degree of improvement was associated with baseline CRP such that higher levels predicted greater decreases. The interaction between gender and baseline CRP was significant and showed that males with higher baseline CRP levels appeared to have a more robust decrease in CRP due to the intervention than did their female counterparts.
It is likely that the vegetable and high fiber content of a vegan diet reduces CRP in the presences of obesity. Neither the quantity of exercise nor the length of stay was significant predictors of CRP reduction. Additionally, those participants who had a vegan diet prior to the intervention had the lowest CRP risk coming into the program. Direct measure of body fat composition, estrogen and other inflammatory mediators such as IL-6 and TNF-alpha would enhance current understanding of the specific mechanisms of CRP reduction related to lifestyle interventions.
Source : Complementary Therapies in Medicine
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Fructose More Toxic than Table Sugar in Mice
Sensitive Toxicity Test Used Sugars in Doses Like What We Eat
When University of Utah biologists fed mice sugar in doses proportional to what many people eat, the fructose-glucose mixture found in high-fructose corn syrup was more toxic than sucrose or table sugar, reducing both the reproduction and lifespan of female rodents.
“This is the most robust study showing there is a difference between high-fructose corn syrup and table sugar at human-relevant doses,” says biology professor Wayne Potts, senior author of a new study scheduled for publication in the March 2015 issue of The Journal of Nutrition.
The study found no differences in survival, reproduction or territoriality of male mice on the high-fructose and sucrose diets. The researchers say that may be because both sugars are equally toxic to male mice.
Both high-fructose corn syrup found in many processed foods and table sugar found in baked goods contain roughly equal amounts of fructose and glucose. But in corn syrup, they are separate molecules, called monosaccharides. In contrast, sucrose or table sugar is a disaccharide compound formed when fructose and glucose bond chemically.
Potts says the debate over the relative dangers of fructose and sucrose is important “because when the diabetes-obesity-metabolic syndrome epidemics started in the mid-1970s, they corresponded with both a general increase in consumption of added sugar and the switchover from sucrose being the main added sugar in the American diet to high-fructose corn syrup making up half our sugar intake.”
James Ruff, the study’s first author and a postdoctoral fellow in biology, says, “Our previous work and plenty of other studies have shown that added sugar in general is bad for your health. So first, reduce added sugar across the board. Then worry about the type of sugar, and decrease consumption of products with high-fructose corn syrup.”
The new study is the latest in a series that used a new, sensitive toxicity test developed by Potts and colleagues. It allows house mice to compete in the seminatural environment of room-size “mouse barns.” Previous mouse studies with the test found harmful effects of inbreeding, the antidepressant Paxil and, last year, an added-sugar diet with fructose and glucose in amounts proportional to a healthy human diet plus three cans of soda daily. These health effects had been missed by conventional tests.
Potts and Ruff ran the new study with former University of Utah undergraduates Sara Hugentobler, Amanda Suchy, Mirtha Sosa, Ruth Tanner and Megumi Hite; and lab manager Linda Morrison. The other coauthors were nutrition researchers Sin Gieng and Mark Shigenaga at Children’s Hospital Oakland Research Institute in California.
The research was funded by the National Institutes of Health and National Science Foundation.
New Findings Build on 2013 Sugar Toxicity Study
The 2013 study found that when mice were fed either a diet with 25 percent calories in the form of added fructose and glucose monosaccharides or 25 percent calories from starch, females died at twice the normal rate and males were a quarter less likely to hold territory and reproduce.
The new study compared two groups of mice that were fed a healthy diet with 25 percent calories from processed sugars. One group ate a mix of fructose-glucose monosaccharides like those in high-fructose corn syrup. The other group ate sucrose.
Female mice on the fructose-glucose diet had death rates 1.87 times higher than females on the sucrose diet. They also produced 26.4 percent fewer offspring.
The new study found no differences in males on the two diets in terms of survival, reproduction or ability to compete for territory. But Potts said the 2013 study showed male mice were a quarter less likely to hold territory and reproduce on the fructose-glucose mix compared with starch. That, combined with the new findings, “suggests sucrose is as bad for males as high-fructose corn syrup,” he says.
Ruff says it also is possible that “other factors are more important than the differences between these two diets for the males” – possibly inherited differences in ability to hold territory.
Potts says female mice that ate the fructose-glucose mixture may be more likely to die than male mice because they undergo a bigger metabolic “energy crunch” during such studies: on the day they give birth, they mate and conceive the next litter, so they are nursing their first litter while gestating a second litter.
Regardless of sex, the researchers also found no difference between mice on the two diets when it came to food intake, weight gain or glucose tolerance. Sucrose is broken into fructose and glucose monosaccharides before the body absorbs it. So whatever caused the different mortality and reproduction in females on the two kinds of sugar diets, “it has to happen at the point of absorption or before – not once it is in the bloodstream, liver or brain,” Ruff says.
“So we speculate that the different sugars could favor different microbes in the guts of mice. Other research has shown differences in bacterial communities in the gut to be associated with metabolic diseases in rodents and in humans. It’s possible one form of sugar causes more bacteria to get across your gut than another.”
A Sugary American Diet
An estimated 13 percent to 25 percent of Americans eat a diet that includes 25 percent or more of calories in the form of added sugars – the percentage of added sugars consumed by mice in the new study. “Added sugars” are sugars added during food processing or preparation and not already naturally in food, like in a piece of fruit.
Ruff says that in the American diet, 44 percent of the added sugar is sucrose, 42 percent is high-fructose corn syrup and the remaining 14 percent includes honey, molasses, juice concentrates and agave – all of which also combine fructose and glucose (which also is known as dextrose). Yet worldwide, high-fructose corn syrup represents only about 8 percent of added sugar consumption, he adds.
Ruff says a number of previous studies in rodents and people tied pure fructose consumption to metabolic problems such as insulin resistance, obesity and abnormal cholesterol and triglyceride levels. He says those studies concluded high-fructose corn syrup was worse than sucrose, but most compared sucrose only to fructose instead of a more realistic fructose-glucose mix.
And “the few previous studies used much higher doses of sugars that are not particularly relevant to humans, and the effects were slight or small,” Potts says.
How the Study Was Performed
The mice in the new study were unrelated, house-type mice, rather than inbred lab mice, because the former compete with each other naturally. For about 40 weeks, mice were fed either the healthy diet with 25 percent of total calories as added fructose and glucose monosaccharides or as sucrose.
Then 160 mice were released into six mouse barns to compete for food, territory and mates for 32 weeks. Each of the 377-square-foot mouse barns held eight to 10 male mice and 14 to 20 females.
Each mouse barn was divided by wire mesh into six territories, each with either an open or protected nest box. Males competed for the better territories and protected nests. Implanted radio chips and antennas at feeders kept track of where mice fed and thus the territories they occupied. The researchers periodically checked for and removed dead mice, as well as pups so they would not breed.
After eating different sugar diets before entering the mouse barns, all the mice ate the fructose-glucose monosaccharide diet while competing in the barns, where they roamed together and couldn’t be kept on different diets. If there were harmful effects from the fructose-glucose diet before entering the mouse barns, they might be obscured if all the mice ate the sucrose diet once in the barns.
Source : Newswise
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Dairy products, calcium, and prostate cancer risk: a systematic review and meta-analysis of cohort studies1,2,3,4
- Dagfinn Aune,
- Deborah A Navarro Rosenblatt,
- Doris SM Chan,
- Ana Rita Vieira,
- Rui Vieira,
- Darren C Greenwood,
- Lars J Vatten, and
- Teresa Norat
Background: Dairy product and calcium intakes have been associated with increased prostate cancer risk, but whether specific dairy products or calcium sources are associated with risk is unclear.
Objective: In the Continuous Update Project, we conducted a meta-analysis of prospective studies on intakes of dairy products and calcium and prostate cancer risk.
Design: PubMed and several other databases were searched up to April 2013. Summary RRs were estimated by using a random-effects model.
Results: Thirty-two studies were included. Intakes of total dairy products [summary RR: 1.07 (95% CI: 1.02, 1.12; n = 15) per 400 g/d], total milk [summary RR: 1.03 (95% CI: 1.00, 1.07; n = 14) per 200 g/d], low-fat milk [summary RR: 1.06 (95% CI: 1.01, 1.11; n = 6) per 200 g/d], cheese [summary RR: 1.09 (95% CI: 1.02, 1.18; n = 11) per 50 g/d], and dietary calcium [summary RR: 1.05 (95% CI: 1.02, 1.09; n = 15) per 400 mg/d] were associated with increased total prostate cancer risk. Total calcium and dairy calcium intakes, but not nondairy calcium or supplemental calcium intakes, were also positively associated with total prostate cancer risk. Supplemental calcium was associated with increased risk of fatal prostate cancer.
Conclusions: High intakes of dairy products, milk, low-fat milk, cheese, and total, dietary, and dairy calcium, but not supplemental or nondairy calcium, may increase total prostate cancer risk. The diverging results for types of dairy products and sources of calcium suggest that other components of dairy rather than fat and calcium may increase prostate cancer risk. Any additional studies should report detailed results for subtypes of prostate cancer.
Source : Amercan Journal of Clinical Nutrition
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Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning
- School of Medical Sciences, The University of New South Wales, Sydney, NSW, Australia
- 2School of Psychology, The University of New South Wales, Sydney, NSW, Australia
A range of animal and human data demonstrates that excessive consumption of palatable food leads to neuroadaptive responses in brain circuits underlying reward. Unrestrained consumption of palatable food has been shown to increase the reinforcing value of food and weaken inhibitory control; however, whether it impacts upon the sensory representations of palatable solutions has not been formally tested. These experiments sought to determine whether exposure to a cafeteria diet consisting of palatable high fat foods impacts upon the ability of rats to learn about food-associated cues and the sensory properties of ingested foods. We found that rats fed a cafeteria diet for 2 weeks were impaired in the control of Pavlovian responding in accordance to the incentive value of palatable outcomes associated with auditory cues following devaluation by sensory-specific satiety. Sensory-specific satiety is one mechanism by which a diet containing different foods increases ingestion relative to one lacking variety. Hence, choosing to consume greater quantities of a range of foods may contribute to the current prevalence of obesity. We observed that rats fed a cafeteria diet for 2 weeks showed impaired sensory-specific satiety following consumption of a high calorie solution. The deficit in expression of sensory-specific satiety was also present 1 week following the withdrawal of cafeteria foods. Thus, exposure to obesogenic diets may impact upon neurocircuitry involved in motivated control of behavior.
Source : Frontiers in Psychology
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More than salt, sugars may contribute to high blood pressure
Cardiovascular disease is the number one cause of premature mortality in the developed world, and hypertension is its most important risk factor.
Hypertension was implicated as a primary or contributing factor in more than 348,000 deaths in the US in 2009, with costs to the nation in excess of $50 billion annually. Controlling hypertension is a major focus of public health initiatives, and dietary approaches to address hypertension have historically focused on sodium.
Nonetheless, the potential benefits of sodium reduction are debatable; studies have shown that the reduction in blood pressure achieved by restricting salt is slim.
Recent data encompassing over 100,000 patients indicates that sodium intake between 3-6 g/day is associated with a lower risk of death and cardiovascular events compared with either a higher or lower level of intake. "Thus, guidelines advising restriction of sodium intake below 3 g/day may cause harm," the authors write.
Processed foods happen to be major sources of not just sodium, but also of highly refined carbohydrates: that is, various sugars and the simple starches that give rise to them through digestion. The researchers comment:
"Compelling evidence from basic science, population studies, and clinical trials implicate sugars, and particularly the monosaccharide fructose, as playing a major role in the development of hypertension. Moreover, evidence suggests that sugars in general and fructose in particular may contribute to overall cardiovascular risk through a variety of mechanisms."
Sucrose, or table sugar, is a disaccharide composed of two monosaccharides: glucose and fructose. Sucrose is a common ingredient in industrially processed foods, but not as common as another sweetener: high-fructose corn syrup (HFCS). Whereas sucrose is equal parts fructose and glucose, HFCS has more fructose (usually 55%) than glucose (the remaining 45%) and is the most frequently used sweetener in processed foods - particularly in fruit drinks and sodas.
Ingesting one 24-ounce soft drink has been shown to cause an average maximum increase in blood pressure of 15/9 mm Hg and heart rate of 9 bpm.
The researchers indicate "sugar may be much more meaningfully related to blood pressure than sodium, as suggested by a greater magnitude of effect with dietary manipulation."
Higher sugar intake significantly increases systolic (6.9 mm Hg) and diastolic blood pressure (5.6 mm Hg) in trials of 8 weeks or more in duration. This effect is increased to 7.6/6.1 mm Hg, when studies that received funding from the sugar industry are excluded.
Those who consume 25% or more calories from added sugar have an almost threefold increased risk of death due to cardiovascular disease, according to the research.
Even moderate doses of added sugar for short durations may cause harmCurrent US per capita intake of added sugars is approximately two to eight times higher than current recommendations by the American Heart Association (AHA) and the World Health Organization (WHO). Considering adolescents specifically, current consumption might be as much as six to 16 times higher.
An increase in sympathetic tone from the overconsumption of fructose is one likely mechanism for the sugar's ability to increase heart rate, cardiac output, renal sodium retention and vascular resistance, all of which may interact to elevate blood pressure and increase myocardial oxygen demand.
However, ingestion of sugars - including fructose - in their naturally occurring biological contexts (i.e. as whole fruits) is not harmful and is likely beneficial.
Just as most dietary sodium does not come from the salt shaker, most dietary sugar does not come from the sugar bowl. Dr James DiNicolantonio, from the Department of Preventive Cardiology at Saint Luke's Mid America Heart Institute on Kansas City, MO, concludes:
"Reducing consumption of added sugars by limiting processed foods containing them, made by corporations would be a good place to start."
The evidence shows that even moderate doses of added sugar for short durations may cause substantial harm.
Source : Medical News Today
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Anti-inflammatory properties of culinary herbs and spices that ameliorate the effects of metabolic syndrome
Alois Jungbauer , Svjetlana Medjakovic
Department of Biotechnology and Christian Doppler Laboratory of Receptor Biotechnology, University of Natural Resources and Life Sciences Vienna, Muthgasse 18, 1190 Vienna, Austria
Obesity and metabolic syndrome are increasing global health problems. In addition to the malnutrition of a sedentary lifestyle, high calorie intake leads to obesity with many negative health consequences. Macrophages infiltrate adipose tissue and induce chronic inflammation by secreting pro-inflammatory cytokines, including COX-2 and iNOS, among other mediators of inflammation. Free fatty acids mediate adipose tissue signalling through toll-like receptor 4 and the expression of these pro-inflammatory mediators via NF-κB or JNK. PPAR γ activators can inhibit the activation of NF-κB, down-regulating the expression of pro-inflammatory cytokines. Here we provide an overview of how different culinary herbs and spices exert anti-inflammatory activities and the extent to which they activate PPAR α and PPAR γ, inhibit the activation of NF-κB, and enhance expression of anti-inflammatory cytokines. Spices can play essential roles as anti-inflammatory agents in our diet, acting as pan PPAR activators and improving insulin sensitivity, counteracting dyslipidaemia and weight gain. The effects of chronic inflammation caused by obesity are counteracted and, consequently, the progression of diseases associated with chronic inflammation slowed.
Source : Journal Maturitas
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Spices and Herbs May Improve Cardiovascular Risk Factors
West, Sheila G. PhD; Skulas-Ray, Ann C. PhD
Sheila G. West, PhD, is professor of biobehavioral health and nutritional sciences at The Pennsylvania State University, University Park.
Ann C. Skulas-Ray, PhD, is a research associate in the department of nutritional sciences at The Pennsylvania State University, University Park.
Traditional risk factors for cardiovascular disease (CVD) include high blood low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, high blood pressure, smoking, and diabetes. Family history and inflammatory factors also affect CVD risk. Diet therapy for treating and managing patients with CVD and for reducing risk among healthy individuals focuses on consuming a diet containing vegetables and fruits; eating whole-grain breads and cereals; choosing poultry, fish, nuts, legumes, and low-fat dairy foods; and limiting the intake of saturated fat, trans-fat, sweets, sugar-sweetened beverages, and red meats.1Because spices and herbs are rich in potentially bioactive compounds, clinical studies have examined their effects on blood insulin, blood lipids, and inflammation.
Spices and herbs are rich in compounds that may reduce inflammation and improve blood factors associated with increased CVD risk. However, the body of literature regarding their effects is small, and the clinical findings are not always consistent. The vascular effects of spices and herbs and their efficacy and safety relative to traditional drug therapy represent an exciting area for future research given the public health significance of CVD.
Source : Nutrition Today
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Milk intake and risk of mortality and fractures in women and men: cohort studies
- Karl Michaëlsson, professor1,
- Alicja Wolk, professor2,
- Sophie Langenskiöld, senior lecturer3,
- Samar Basu, professor3,
- Eva Warensjö Lemming, researcher14,
- Håkan Melhus, professor5,
- Liisa Byberg, associate professor1
Objective To examine whether high milk consumption is associated with mortality and fractures in women and men.
Design Cohort studies.
Setting Three counties in central Sweden.
Participants Two large Swedish cohorts, one with 61 433 women (39-74 years at baseline 1987-90) and one with 45 339 men (45-79 years at baseline 1997), were administered food frequency questionnaires. The women responded to a second food frequency questionnaire in 1997.
Main outcome measure Multivariable survival models were applied to determine the association between milk consumption and time to mortality or fracture.
Results During a mean follow-up of 20.1 years, 15 541 women died and 17 252 had a fracture, of whom 4259 had a hip fracture. In the male cohort with a mean follow-up of 11.2 years, 10 112 men died and 5066 had a fracture, with 1166 hip fracture cases. In women the adjusted mortality hazard ratio for three or more glasses of milk a day compared with less than one glass a day was 1.93 (95% confidence interval 1.80 to 2.06). For every glass of milk, the adjusted hazard ratio of all cause mortality was 1.15 (1.13 to 1.17) in women and 1.03 (1.01 to 1.04) in men. For every glass of milk in women no reduction was observed in fracture risk with higher milk consumption for any fracture (1.02, 1.00 to 1.04) or for hip fracture (1.09, 1.05 to 1.13). The corresponding adjusted hazard ratios in men were 1.01 (0.99 to 1.03) and 1.03 (0.99 to 1.07). In subsamples of two additional cohorts, one in males and one in females, a positive association was seen between milk intake and both urine 8-iso-PGF2α (a biomarker of oxidative stress) and serum interleukin 6 (a main inflammatory biomarker).
Conclusions High milk intake was associated with higher mortality in one cohort of women and in another cohort of men, and with higher fracture incidence in women. Given the observational study designs with the inherent possibility of residual confounding and reverse causation phenomena, a cautious interpretation of the results is recommended.
Source : British Medical Journal
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Weight loss effects from vegetable intake: a 12-month randomised controlled trial
L C Tapsell1, M J Batterham1, R L Thorne1, J E O'Shea1, S J Grafenauer1 and Y C Probst1
1School of Medicine, Smart Foods Centre, Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, New South Wales, Australia
Background/Objectives: Direct evidence for the effects of vegetable intake on weight loss is qualified. The study aimed to assess the effect of higher vegetable consumption on weight loss.
Subjects/Methods: A single blind parallel controlled trial was conducted with 120 overweight adults (mean body mass index=29.98 kg/m2) randomised to two energy deficit healthy diet advice groups differing only by doubling the serving (portion) sizes of vegetables in the comparator group. Data were analysed as intention-to-treat using a linear mixed model. Spearmans rho bivariate was used to explore relationships between percentage energy from vegetables and weight loss.
Results: After 12 months, the study sample lost 6.5±5.2 kg (P<0.001 time) with no difference between groups (P>0.05 interaction). Both groups increased vegetable intake and lost weight in the first 3 months, and the change in weight was significantly correlated with higher proportions of energy consumed as vegetables (rho=–0.217, P=0.024). Fasting glucose, insulin and triglyceride levels decreased (P<0.001 time) and high-density lipoprotein cholesterol levels increased (P<0.001 time), with no difference between groups. Weight loss was sustained for 12 months by both groups, but the comparator group reported greater hunger satisfaction (P=0.005).
Conclusions: Advice to consume a healthy low-energy diet leads to sustained weight loss, with reductions in cardiovascular disease risk factors regardless of an emphasis on more vegetables. In the short term, consuming a higher proportion of the dietary energy as vegetables may support a greater weight loss and the dietary pattern appears sustainable.
Source : European Journal of Clinical Nutrition
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Dietary Patterns in Children with Attention Deficit/Hyperactivity Disorder (ADHD)
Hae Dong Woo 1, Dong Woo Kim 1, Young-Seoub Hong 2,3, Yu-Mi Kim 2,3, Ju-Hee Seo 3, Byeong Moo Choe 4, Jae Hong Park 4, Je-Wook Kang 5, Jae-Ho Yoo 6, Hee Won Chueh 6, Jung Hyun Lee 7, Min Jung Kwak 8 and Jeongseon Kim 1,*
Abstract: The role of diet in the behavior of children has been controversial, but the association of several nutritional factors with childhood behavioral disorders has been continually suggested. We conducted a case-control study to identify dietary patterns associated with attention deficit hyperactivity disorder (ADHD). The study included 192 elementary school students aged seven to 12 years. Three non-consecutive 24-h recall (HR) interviews were employed to assess dietary intake, and 32 predefined food groups were considered in a principal components analysis (PCA). PCA identified four major dietary patterns: the “traditional” pattern, the “seaweed-egg” pattern, the “traditional-healthy” pattern, and the “snack” pattern. The traditional-healthy pattern is characterized by a diet low in fat and high in carbohydrates as well as high intakes of fatty acids and minerals. The multivariate-adjusted odds ratio (OR) of ADHD for the highest tertile of the traditional-healthy pattern in comparison with the lowest tertile was 0.31 (95% CI: 0.12–0.79). The score of the snack pattern was positively associated with the risk of ADHD, but a significant association was observed only in the second tertile. A significant association between ADHD and the dietary pattern score was not found for the other two dietary patterns. In conclusion, the traditional-healthy dietary pattern was associated with lower odds having ADHD
Source : Journal Nutritents
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Dietary protein sources in early adulthood and breast cancer incidence: prospective cohort study
Objective To investigate the association between dietary protein sources in early adulthood and risk of breast cancer.
Design Prospective cohort study.
Setting Health professionals in the United States.
Participants 88 803 premenopausal women from the Nurses’ Health Study II who completed a questionnaire on diet in 1991.
Main outcome measure Incident cases of invasive breast carcinoma, identified through self report and confirmed by pathology report.
Results We documented 2830 cases of breast cancer during 20 years of follow-up. Higher intake of total red meat was associated with an increased risk of breast cancer overall (relative risk 1.22, 95% confidence interval 1.06 to 1.40; Ptrend=0.01, for highest fifth v lowest fifth of intake). However, higher intakes of poultry, fish, eggs, legumes, and nuts were not related to breast cancer overall. When the association was evaluated by menopausal status, higher intake of poultry was associated with a lower risk of breast cancer in postmenopausal women (0.73, 0.58 to 0.91; Ptrend=0.02, for highest fifth v lowest fifth of intake) but not in premenopausal women (0.93, 0.78 to 1.11; Ptrend=0.60, for highest fifth v lowest fifth of intake). In estimating the effects of exchanging different protein sources, substituting one serving/day of legumes for one serving/day of red meat was associated with a 15% lower risk of breast cancer among all women (0.85, 0.73 to 0.98) and a 19% lower risk among premenopausal women (0.81, 0.66 to 0.99). Also, substituting one serving/day of poultry for one serving/day of red meat was associated with a 17% lower risk of breast cancer overall (0.83, 0.72 to 0.96) and a 24% lower risk of postmenopausal breast cancer (0.76, 0.59 to 0.99). Furthermore, substituting one serving/day of combined legumes, nuts, poultry, and fish for one serving/day of red meat was associated with a 14% lower risk of breast cancer overall (0.86, 0.78 to 0.94) and premenopausal breast cancer (0.86, 0.76 to 0.98).
Conclusion Higher red meat intake in early adulthood may be a risk factor for breast cancer, and replacing red meat with a combination of legumes, poultry, nuts and fish may reduce the risk of breast cancer.
Source : BMJ
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Nutrition and the Risk of Alzheimer's Disease
Nan Hu,1 Jin-Tai Yu,1,2 Lin Tan,1 Ying-Li Wang,1 Lei Sun,1 and Lan Tan1,2
1Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Number 5 Donghai Middle Road, Qingdao 266071, China
2College of Medicine and Pharmaceutics, Ocean University of China, Qingdao 266003, China
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that accounts for the major cause of dementia, and the increasing worldwide prevalence of AD is a major public health concern. Increasing epidemiological studies suggest that diet and nutrition might be important modifiable risk factors for AD. Dietary supplementation of antioxidants, B vitamins, polyphenols, and polyunsaturated fatty acids are beneficial to AD, and consumptions of fish, fruits, vegetables, coffee, and light-to-moderate alcohol reduce the risk of AD. However, many of the results from randomized controlled trials are contradictory to that of epidemiological studies. Dietary patterns summarizing an overall diet are gaining momentum in recent years. Adherence to a healthy diet, the Japanese diet, and the Mediterranean diet is associated with a lower risk of AD. This paper will focus on the evidence linking many nutrients, foods, and dietary patterns to AD.
Source : Biomed Research International
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Meat Consumption as a Risk Factor for Type 2 Diabetes
Neal Barnard,1 Susan Levin,2,* and Caroline Trapp2
Disease risk factors identified in epidemiological studies serve as important public health tools, helping clinicians identify individuals who may benefit from more aggressive screening or risk-modification procedures, allowing policymakers to prioritize intervention programs, and encouraging at-risk individuals to modify behavior and improve their health. These factors have been based primarily on evidence from cross-sectional and prospective studies, as most do not lend themselves to randomized trials. While some risk factors are not modifiable, eating habits are subject to change through both individual action and broader policy initiatives. Meat consumption has been frequently investigated as a variable associated with diabetes risk, but it has not yet been described as a diabetes risk factor. In this article, we evaluate the evidence supporting the use of meat consumption as a clinically useful risk factor for type 2 diabetes, based on studies evaluating the risks associated with meat consumption as a categorical dietary characteristic (i.e., meat consumption versus no meat consumption), as a scalar variable (i.e., gradations of meat consumption), or as part of a broader dietary pattern.
Source : Journal Nutrients
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Acid Levels in the Diet Could Have Profound Effects on Kidney Health
Three new studies suggest that controlling dietary acid intake could help improve kidney health. Results of these studies will be presented at ASN Kidney Week 2013 November 5¬–10 at the Georgia World Congress Center in Atlanta, GA.
A diet rich in wheat flour and animal protein produces an acidic environment in the body that worsens with age as kidney function declines. This acid load can be detrimental to a variety of tissues and processes. Research suggests that consuming more fruits and vegetables—which are highly alkaline—may help counteract these effects.
In a new study, a team led by Nimrit Goraya, MD (Texas A&M College of Medicine) investigated whether consuming fruits and vegetables can protect the kidney health of individuals with hypertensive nephropathy, a condition in which damage to the kidneys occurs due to high blood pressure. In this study, 23 hypertensive patients received extra dietary fruits and vegetables, 23 patients received an oral alkaline medication, and 25 patients received nothing. One year later, kidney injury progressed in patients who received no intervention, but kidney health was preserved in those receiving fruits and vegetables or oral alkaline medication.
In another study, Eiichiro Kanda, MD, PhD (Tokyo Kyosai Hospital) and his colleagues investigated the role of dietary acid levels in chronic kidney disease (CKD) progression. The retrospective study analyzed data from 249 CKD patients in Japan. High acid levels were linked with accelerated kidney function decline, and patients with elevated acid levels had an increased risk of CKD progression compared with patients with low acid levels. The findings suggest that monitoring and control of dietary acid levels are necessary for the prevention of CKD progression.
Another study led by Deidra Crews, MD, FASN (Johns Hopkins University School of Medicine) looked to see whether the effect of dietary acid on risk of kidney failure differed by race in a group of 159 non-Hispanic black and 760 non-Hispanic white CKD patients who had an annual household income below 300% of the federal poverty guideline. Participants were taking part in the 1999-2004 National Health and Nutrition Examination Survey. Overall, 12.4% of participants (38.3% whites and 61.7% blacks) developed kidney failure during an average of 6.4 years of follow up. Blacks had higher acid levels than whites. They also had a 3-fold higher risk of developing kidney failure compared with whites after adjusting for factors such as age, sex, and caloric intake. Increased acid levels were more strongly associated with kidney failure among blacks than among whites. The findings indicate that among CKD patients with low socioeconomic status, the detrimental effect of high dietary acid levels on progression to kidney failure appears to be greater for blacks than for whites.
Source : Newswise
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Meat consumption and mortality - results from the European Prospective Investigation into Cancer and Nutrition
Sabine Rohrmann1,2*, Kim Overvad3, H B Bueno-de-Mesquita4,5, Marianne U Jakobsen3, Rikke Egeberg6, Anne Tjønneland6, Laura Nailler7,8, Marie-Christine Boutron-Ruault7,8, Françoise Clavel-Chapelon7,8, Vittorio Krogh9, Domenico Palli10, Salvatore Panico11, Rosario Tumino12, Fulvio Ricceri13, Manuela M Bergmann14, Heiner Boeing14, Kuanrong Li2, Rudolf Kaaks2, Kay-Tee Khaw15, Nicholas J Wareham16, Francesca L Crowe17, Timothy J Key17, Androniki Naska18, Antonia Trichopoulou18,19, Dimitirios Trichopoulos19,20,21, Max Leenders5, Petra HM Peeters22,23, Dagrun Engeset24, Christine L Parr25, Guri Skeie24, Paula Jakszyn26, María-José Sánchez27,28, José M Huerta27,29, M L Redondo30, Aurelio Barricarte28,31, Pilar Amiano28,32, Isabel Drake33, Emily Sonestedt33, Göran Hallmans34, Ingegerd Johansson35, Veronika Fedirko36, Isabelle Romieux36, Pietro Ferrari36, Teresa Norat23, Anne C Vergnaud23, Elio Riboli23 and Jakob Linseisen2,37
1. Division of Cancer Epidemiology and Prevention, Institute of Social and Preventive Medicine, University of Zurich, 8001 Zurich, Switzerland
2 Division of Cancer Epidemiology, Deutsches Krebsforschungszentrum, 69221 Heidelberg, Germany
3 Section of Epidemiology, Department of Public Health, Aarhus University, 8000 Aarhus, Denmark
4 National Institute for Public Health and the Environment (RIVM), 3720 Bilthoven, The Netherlands
5 Department of Gastroenterology and Hepatology, University Medical Centre, 3508 Utrecht, The Netherlands
6 Danish Cancer Society Research Center, 2100 Copenhagen, Denmark
7 Inserm, Centre for Research in Epidemiology and Population Health, U1018, Institut Gustave Roussy, 94805 Villejuif, France
8 Paris South University, UMRS 1018, 94805 Villejuif, France
9 Nutritional Epidemiology Unit, Fondazione IRCCS Istituto Nazionale Tumori, 20133 Milan, Italy
10 Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute (ISPO), 50139 Florence, Italy
11 Department of Clinical and Experimental Medicine, Federico II University, 80131 Naples, Italy
12 Cancer Registry and Histopathology Unit, "Civile - M.P.Arezzo" Hospital, 97100 Ragusa, Italy
13 HuGeF - Human Genetics Foundation - Torino, 10126 Torino, Italy
14 Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbrücke, 14558 Nuthetal, Germany
15 Department of Public Health and Primary Care, University of Cambridge, Cambridge CB2 2QQ, UK
16 Medical Research Council (MRC) Epidemiology Unit, Cambridge CB2 0QQ, UK
17 Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, University of Oxford, Oxford OX3 7LF, UK
18 WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology and Medical Statistics, University of Athens Medical School, 11527 Athens, Greece
19 Hellenic Health Foundation, 11527 Athens, Greece
20 Department of Epidemiology, Harvard School of Public Health, Boston MA 02115, USA
21 Bureau of Epidemiologic Research, Academy of Athens, 11527 Athens, Greece
22 Julius Center, University Medical Center Utrecht, 3508 Utrecht, The Netherlands
23 School of Public Health, Imperial College, London SW7 2AZ, UK
24 Department of Community Medicine, University of Tromsø, 9037 Tromsø, Norway
25 Department of Biostatistics, Faculty of Medicine, University of Oslo, 0317 Oslo, Norway
26 Unit of Nutrition, Environment and Cancer, Cancer Epidemiology Research Program, Catalan Institute of Oncology (ICO), 08907 Barcelona, Spain
27 Andalusian School of Public Health, 18080 Granada, Spain
28 Consortium for Biomedical Research in Epidemiology and Public Health (CIBER Epidemiología y Salud Pública-CIBERESP), pain
29 Department of Epidemiology, Murcia Regional Health Council, 30008 Murcia, Spain
30 Public Health Directorate Asturias, 33006 Oviedo, Spain
31 Navarre Public Health Institute, 31003 Pamplona, Spain
32 Public Health Division of Gipuzkoa, BIODonostia Research Institute, Department of Health of the Regional Government of the Basque Country, San Sebastian, Spain
33 Department of Clinical Sciences, Lund University, 20502 Malmö, Sweden
34 Department of Public Health and Clinical Medicine, Nutrition Research, 90185 Umeå University, Umeå, Sweden
35 Department of Odontology, Cariology, Umeå University, 90185 Umeå, Sweden
36 International Agency for Research on Cancer (IARC), 69008 Lyon, France
37 Institute of Epidemiology, Helmholtz Centre Munich, 85764 Neuherberg, Germany
Recently, some US cohorts have shown a moderate association between red and processed meat consumption and mortality supporting the results of previous studies among vegetarians. The aim of this study was to examine the association of red meat, processed meat, and poultry consumption with the risk of early death in the European Prospective Investigation into Cancer and Nutrition (EPIC).
Included in the analysis were 448,568 men and women without prevalent cancer, stroke, or myocardial infarction, and with complete information on diet, smoking, physical activity and body mass index, who were between 35 and 69 years old at baseline. Cox proportional hazards regression was used to examine the association of meat consumption with all-cause and cause-specific mortality.
As of June 2009, 26,344 deaths were observed. After multivariate adjustment, a high consumption of red meat was related to higher all-cause mortality (hazard ratio (HR) = 1.14, 95% confidence interval (CI) 1.01 to 1.28, 160+ versus 10 to 19.9 g/day), and the association was stronger for processed meat (HR = 1.44, 95% CI 1.24 to 1.66, 160+ versus 10 to 19.9 g/day). After correction for measurement error, higher all-cause mortality remained significant only for processed meat (HR = 1.18, 95% CI 1.11 to 1.25, per 50 g/d). We estimated that 3.3% (95% CI 1.5% to 5.0%) of deaths could be prevented if all participants had a processed meat consumption of less than 20 g/day. Significant associations with processed meat intake were observed for cardiovascular diseases, cancer, and 'other causes of death'. The consumption of poultry was not related to all-cause mortality.
The results of our analysis support a moderate positive association between processed meat consumption and mortality, in particular due to cardiovascular diseases, but also to cancer.
Source : BMC Medicine
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Eating for Eye Health Can Be Beneficial
Eating healthy can affect more than what the scale says. According to experts at the University of Alabama at Birmingham (UAB), it is possible to aid eye health through nutrition and supplements.Research by the National Eye Institute (NEI) has shown that high levels of antioxidants and zinc, in the form of a nutritional supplement tablet, reduced the risk of advanced age-related macular degeneration (AMD).
“AMD is the leading cause of blindness in older adults,” said Cynthia Owsley, Ph.D., professor and vice chair for clinical research in the Department of Ophthalmology. “These dietary supplements are not a cure for AMD, but they do reduce one’s risk of progressing to the most serious form of the disease.”
UAB School of Optometry Professor Leo Semes, O.D., talked about the importance of diet to eye health.
“You are what you eat; it’s trite but it’s true,” Semes said. “It’s been shown that certain habits like eating a high-fat diet are associated with, but not causative, in AMD.”
One food that has long been connected with improving vision is carrots, but Semes said carrots alone will not accomplish significant gains in eye health.
“The basis for this belief is that carrots are high in beta-carotene,” Semes said. “But beta-carotene alone is not going to be protective enough. There’s also a tangential relationship that a lack of vitamin-A, a cousin of beta-carotene, is implicated in poor darkness adaptation.”
Seeing well when moving from light to dark declines with age.
Semes serves on the American Optometric Association Health and Nutrition Committee, which developed a list of specific foods and nutrients that have been found to be beneficial to eye health.
• Fruits and vegetables – Vitamin C can help minimize cataracts and AMD
• Fleshy fish (tuna or salmon) and lean meats – Fatty acids protect against AMD
• Red meats and whole grains – Zinc deficiency can lead to cataracts
• Vegetable oil – Vitamin E can slow progression of AMD
Source : Newswise
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Healthy Eating Beneficial Beyond Drug Therapy in Preventing a Second Heart Attack
A heart-healthy diet rich in fruits, vegetables and fish significantly reduces the chance of a second heart attack and stroke in people with cardiovascular disease, McMaster University researchers have found.A five-year study of almost 32,000 patients (average age 66.5 years) in 40 countries discovered those who ate a heart-healthy diet had a:
. 35 per cent reduction in risk for cardiovascular death
. 14 per cent reduction in risk for new heart attacks
. 28 per cent reduction in risk for congestive heart failure
. 19 per cent reduction in risk for stroke
“At times, patients don’t think they need to follow a healthy diet since their medications have already lowered their blood pressure and cholesterol – that is wrong,” said Mahshid Dehghan, the study’s lead author and nutritionist at McMaster University’s Population Health Research Institute (PHRI). “Dietary modification has benefits in addition to those seen with Aspirin, angiotensin modulators, lipid-lowering agents and beta blockers.”
The study is posted on-line today in the American Heart Association Rapid Access Journal.
Each year, at least 20 million people worldwide survive a heart attack or stroke. While drug treatments, such as Aspirin, substantially lower their risk of another heart attack, the McMaster study is the first to show a high quality diet also significantly lowers their risk.
For the study, researchers assessed the association between diet quality and the risk of cardiovascular disease using information collected from men and women who participated in two major McMaster-led global studies: ONTARGET, and TRANSCEND.
Participants with cardiovascular disease were asked how often they consumed milk, vegetables, fruits, grains, fish, nuts, meat and poultry over the past 12 months. They were also asked about lifestyle choices such as alcohol consumption, smoking and exercise. A healthy diet was indicated by a high intake of fruits, vegetables, whole grains and nuts as well as a high intake of fish compared to meat, poultry and eggs.
Researchers found a heart-healthy diet offered a “consistent benefit” over and above the benefits of taking medications to reduce the risk of heart attack and stroke.
Globally, healthy eating was associated with a lower risk of cardiovascular disease by more than 20 per cent in all regions of the world, which were grouped based on their food habit. According to income, similar results were found in middle and high income countries in different regions of the world.
The researchers believe this is the first study to report on the protective impact of healthy eating for individuals with cardiovascular disease who are taking medication to prevent a second heart attack, stroke or death.
“Physicians should advise their high-risk patients to improve their diet and eat more vegetables, fruits, grains and fish,” Dehghan said. “This could substantially reduce cardiovascular recurrence beyond drug therapy alone and save lives globally.”
Source : Newswise
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Influence of parents and friends on children's and adolescents' food intake and food selection1,2,3
Sarah-Jeanne Salvy, Alison Elmo, Lauren A Nitecki, Melissa A Kluczynski, and James N Roemmich
Background: The influence of parents versus friends on youths' eating behavior has not been directly compared, and little is known about the developmental effects of social influences on their eating behavior.
Objective: The objective was to compare the effects of mothers and friends on children's and adolescents' energy intake from sandwiches and from healthy and unhealthy snacks and dessert foods.
Design: Twenty-three children (ages 5–7 y) and 27 adolescents (ages 13–15 y) ate a meal with their mother on one occasion and with a same-sex friend on another occasion.
Results: Male and female children consumed less energy from unhealthy snacks when in the presence of their mothers than when in the company of their friends. Conversely, female adolescents consumed less energy from unhealthy snacks and more energy from healthy snacks when they were with their friends than when with their mothers.
Conclusions: Food selection is differentially influenced by the source of social influence and the age and sex of the child. Parents may act as an inhibitory influence on unhealthy eating for younger children. Adolescent girls may try to convey a good impression of healthy eating when eating with same-sex friends, but the eating habits of teenage boys are not as influenced by the social context.
Source : The American Journal of Clinical Nutrition
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