Los polifenoles de la granada prevendrían de la enfermedad coronaria – correofarmacéutico.com
El estudio llevado a cabo por el Hospital de la Santa Cruz y San Pablo de Barcelona, ha consistido en la alimentación de un grupo de animales durante diez días con un pienso estándar para cerdos y a otro grupo con una dieta rica en grasas saturadas y colesterol para poder obtener niveles de colesterol similares a los que se observan en la dislipemia humana y, que a su vez, inducirían a la disfunción endotelial, con una administración a la mitad de los animales de cada uno de los dos grupos con la dieta de un suplemento de 625mg/día con extracto de granada.
Los resultados señalaron que tras diez días y una hora después de ingerir la dieta, los investigadores demostraron que los animales con una dieta rica en grasas saturadas y colesterol presentaron una reducción de vasodilatación del 50 por ciento y que los animales que recibieron un suplemento con extracto de granada mostraron una capacidad de vasodilatación similar a la del grupo de animales con pienso estándar.
Asimismo, Gemma Vilahur, coautora del estudio e investigadora del Centro de Investigación Cardiovascular (CSIC-ICCC) del Hospital de la Santa Cruz y San Pablo de Barcelona, ha destacado que “otro dato observado ha sido que las lipoproteínas de alta densidad (HDL) mostraron mayor capacidad antioxidante y las lipoproteínas de baja densidad (LDL) fueron más resistentes a la oxidación después de la ingesta del suplemento de granada”.
October 22, 2014Drinking milk produced from sources other than cows may increase the risk for low levels of serum vitamin D in young children compared with drinking cow’s milk, according to a study published online October 20 in the Canadian Medical Association Journal.
Although fortification of cow’s milk with vitamin D is required in the United States and Canada, fortification of non-cow’s milk is voluntary.
Grace J. Lee, BASc, from the University of Toronto, Ontario, Canada, and colleagues conducted a cross-sectional study of children between 1 and 6 years old recruited from seven pediatric or family medicine primary care practices during well-child visits between December 2008 and September 2013. The practices are in the network collaboration of the Faculty of Medicine, the Department of Paediatrics, and the Department of Family and Community Medicine at the University of Toronto.
The researchers compared levels of serum 25-hydroxyvitamin D in 2468 children who drink cow’s milk with levels in 363 children who drink goat’s milk or plant-based milk. Researchers collected data through physical measurements, blood samples, and interviews with parents.
Mean age of participants was 2.9 years, and the children were split almost equally between boys and girls.
The median vitamin D level was 80 nmol/L in the entire study population, 81 nmol/L in those drinking just cow’s milk (n = 1950), and 78 nmol/L in those drinking only non-cow’s milk (n = 146).
However, the vitamin D level was below 50 nmol/L in 4.7% of those who drank only cow’s milk and in 11.0% of those who drank only non-cow’s milk. Using logistic regression analysis, the researchers found that children who drank only non-cow’s milk were almost three times as likely as children who drank cow’s milk to have vitamin D levels lower than 50 nmol/L (odds ratio, 2.7; 95% confidence interval, 1.6 – 4.7).
Overall, in an unadjusted analysis, researchers found that a 3.1% decrease (P = .005) in vitamin D level occurred for each 250-mL cup of non-cow’s milk consumed.
“Among children who drank both types of milk, each additional cup of non–cow’s milk beverage consumed was associated with a 5% decrease in 25-hydroxyvitamin D level,” the researchers write. The estimated was adjusted for clinically relevant variables, the authors note.
They conclude, “Our findings may be helpful for health care providers caring for children who drink non–cow’s milk beverages because of an allergy to cow’s milk, lactose intolerance or a dietary preference.”
The authors have disclosed no relevant financial relationships.
CMAJ. Published online October 20, 2014. Abstract
La deficiencia de vitamina D está más vinculada a la diabetes que a la obesidad – DiarioMedico.com
January 05, 2015
Are there particular populations of adults for whom you would recommend screening, or vitamin D supplementation in the absence of screening?
![]() |
Response from David B. Reuben, MD Professor and Archstone Foundation Endowed Chair, Department of Medicine, University of California Los Angeles; Chief, Division of Geriatrics, UCLA Medical Center, Santa Monica, California |
Several prospective epidemiologic studies have shown associations of low serum vitamin D levels with lower global cognition and more rapid functional decline,[1-4] as well as the development of dementia and Alzheimer disease.[5] In a recent review of nine epidemiologic studies, the serum level that was associated with worse cognitive health was found to be around 10 ng/mL.[1] However, such studies cannot determine whether low vitamin D was causal or whether persons with memory problems were less likely to leave their homes and therefore have less sun exposure, leading to lower vitamin levels.
It is less clear whether and how much vitamin D supplementation would improve cognition or prevent decline in older populations. To date, there are no randomized clinical trial data supporting supplementation for improving cognition or preventing decline.
In the Women’s Health Initiative Memory Study, calcium and 400 IU vitamin D3 supplements given to a randomized sample of women did not result in differences in performance (attention, working memory, word knowledge, spatial ability, verbal fluency, verbal memory, figural memory, or fine motor speed) over 7.8 years.[6] Moreover, in observational studies, high levels of 25-hydroxyvitamin D, especially among those taking vitamin D supplements, have been associated with cognitive impairment on a battery of attention tests, suggesting a possible U-shaped curve relationship.[7]
Recently, the US Preventive Services Task Force has reviewed the evidence for screening for vitamin D deficiency and concluded that the current evidence is “insufficient to assess the balance of benefits and harms of screening for vitamin D deficiency in asymptomatic adults.”[8] Part of the rationale for this recommendation stemmed from the paucity of studies that used an internationally recognized reference standard and the lack of consensus on the laboratory values that define vitamin D deficiency.
In summary, the best evidence supports the recommendation of daily dietary vitamin D intake of 600 IU in adults aged 18-70 years and 800 IU in adults older than 70 years (1000 IU is commonly marketed).[9] Vitamin D levels should be obtained in patients with symptoms of osteomalacia (eg, diffuse bone and joint pain, fractures, muscle weakness, and difficulty walking), especially in malabsorption states, and before starting intravenous bisphosphonate therapy for osteoporosis because of the potential for precipitating hypocalcemia in patients with hypovitaminosis D receiving these medications. Currently, there is no indication for screening asymptomatic patients for vitamin D levels for the purpose of potentially supplementing with vitamin D in order to prevent changes in cognitive outcomes.
Developed in association with the UCLA Alzheimer’s and Dementia Care Program.
January 08, 2015 (Reuters Health) – People who get a lot of antioxidants in their diets, or who take them in supplement form, don’t live any longer than those who just eat well overall, according to a long term study of retirees in California.
Annlia Paganini-Hill of the Clinic for Aging Research and Education at the University of California, Irvine and colleagues analyzed mailed surveys from the 1980s in which almost 14,000 older residents of the Leisure World Laguna Hills retirement community detailed their intake of 56 foods or food groups rich in vitamins A and C as well as their vitamin supplement intake.
Two-thirds of the original group took vitamin supplements, most often vitamin C. The authors note, though, that the participants’ diets alone were generally more than adequate to meet minimum dietary requirements for vitamin intake.
With periodic check-ins and repeated surveys, the researchers followed the group for the next 32 years, during which time 13,104 residents died.
When Paganini-Hill’s team accounted for smoking, alcohol intake, caffeine consumption, exercise, body mass index, and histories of hypertension, angina, heart attack, stroke, diabetes, rheumatoid arthritis and cancer, there was no association between the amount of vitamins A or C in the diet or vitamin E supplements and the risk of death.
Vitamin users may have different lifestyles or underlying disease states that are related to their risk of death, the authors write.
“In the general population, health-promoting habits often cluster; e.g. those who take vitamin supplements often exercise, do not smoke, and are not obese,” Paganini-Hill told Reuters Health. “Thus, these factors may explain the observed association between longevity and vitamin supplements.”
On the other hand, the authors note, people with unhealthy habits might be more likely to take supplements. For instance, men who were current smokers were about twice as likely to take in high or medium amounts of vitamin C compared to men who had never smoked. A similar pattern held for men’s vitamin A intake and women’s intake of both A and C.
Some large studies have found a connection between vitamin intake and risk of death, but most have not, the study team points out.
“We know quite a lot about how antioxidants act and what they, theoretically, can prevent,” said Sabine Rohrmann of the Institute of Social and Preventive Medicine at the University of Zurich.
“One of the critical issues is that we don’t know very much about how antioxidants act at different concentrations and how they act in humans who have, or who do not have, sufficient vitamin/antioxidant intake,” Rohrmann told Reuters Health by email.
Participants in the new study were largely white, educated and well-nourished.
“We know that the most important factors that influence mortality are smoking and excess body weight,” Rohrmann said. Many studies support the notion that vitamin supplements are usually not necessary because our nutrient intake via a healthy diet is usually sufficient, she said.
Antioxidants can have risks as well. According to the National Institutes of Health, high doses of beta-carotene may increase the risk of lung cancer in smokers, high doses of vitamin E may increase risks of prostate cancer and one type of stroke, and antioxidant supplements may also interact with some medicines.
“Antioxidant supplements should not be used to replace a nutritionally adequate diet,” Paganini-Hill said.
The study was published online December 29 in the American Journal of Epidemiology.
SOURCE: http://bit.ly/1Fgx3a8
Am J Epidemiol 2014.
January 05, 2015
Are there particular populations of adults for whom you would recommend screening, or vitamin D supplementation in the absence of screening?
![]() |
Response from David B. Reuben, MD Professor and Archstone Foundation Endowed Chair, Department of Medicine, University of California Los Angeles; Chief, Division of Geriatrics, UCLA Medical Center, Santa Monica, California |
Several prospective epidemiologic studies have shown associations of low serum vitamin D levels with lower global cognition and more rapid functional decline,[1-4] as well as the development of dementia and Alzheimer disease.[5] In a recent review of nine epidemiologic studies, the serum level that was associated with worse cognitive health was found to be around 10 ng/mL.[1] However, such studies cannot determine whether low vitamin D was causal or whether persons with memory problems were less likely to leave their homes and therefore have less sun exposure, leading to lower vitamin levels.
It is less clear whether and how much vitamin D supplementation would improve cognition or prevent decline in older populations. To date, there are no randomized clinical trial data supporting supplementation for improving cognition or preventing decline.
In the Women’s Health Initiative Memory Study, calcium and 400 IU vitamin D3 supplements given to a randomized sample of women did not result in differences in performance (attention, working memory, word knowledge, spatial ability, verbal fluency, verbal memory, figural memory, or fine motor speed) over 7.8 years.[6] Moreover, in observational studies, high levels of 25-hydroxyvitamin D, especially among those taking vitamin D supplements, have been associated with cognitive impairment on a battery of attention tests, suggesting a possible U-shaped curve relationship.[7]
Recently, the US Preventive Services Task Force has reviewed the evidence for screening for vitamin D deficiency and concluded that the current evidence is “insufficient to assess the balance of benefits and harms of screening for vitamin D deficiency in asymptomatic adults.”[8] Part of the rationale for this recommendation stemmed from the paucity of studies that used an internationally recognized reference standard and the lack of consensus on the laboratory values that define vitamin D deficiency.
In summary, the best evidence supports the recommendation of daily dietary vitamin D intake of 600 IU in adults aged 18-70 years and 800 IU in adults older than 70 years (1000 IU is commonly marketed).[9] Vitamin D levels should be obtained in patients with symptoms of osteomalacia (eg, diffuse bone and joint pain, fractures, muscle weakness, and difficulty walking), especially in malabsorption states, and before starting intravenous bisphosphonate therapy for osteoporosis because of the potential for precipitating hypocalcemia in patients with hypovitaminosis D receiving these medications. Currently, there is no indication for screening asymptomatic patients for vitamin D levels for the purpose of potentially supplementing with vitamin D in order to prevent changes in cognitive outcomes.
Developed in association with the UCLA Alzheimer’s and Dementia Care Program.
Expertos alertan sobre la ingesta de metilmercurio a través del pescado – correofarmacéutico.com
Sobre qué es el metilmercurio y dónde se encuentra, han explicado que la contaminación ambiental del mercurio proviene de fuentes naturales como erupciones volcánicas o emisiones antropogénicas (por ejemplo, la combustión de fósiles). En el ciclo acuático, una vez que el mercurio se ha depositado, se transforma en metilmercurio por la acción de determinadas bacterias y se bioacumula en los organismos acuáticos, incorporándose a la cadena trófica de alimentos.
“Por ello, la fuente de exposición principal al metilmercurio es el consumo de pescado salvaje y marisco contaminado. La Unión Europea estableció un Reglamento con el máximo de mercurio permitido para los productos de la pesca. Concretamente, los peces con mayor contenido de mercurio son los peces grandes depredadores como el emperador, el pez espada, el tiburón, el atún o el marlín”, ha puntualizado la experta.
Además, según se detalla en los documentos elaborados por el Geprem-Hg, de cara al consumo de estos pescados, el contenido de mercurio no se puede eliminar mediante la limpieza ni el cocinado del pescado ya que más del 90 por ciento de su contenido se encuentra en forma de metilmercurio unido a las proteínas, y no en la grasa. La forma en que se encuentra el pescado (fresco, congelado o enlatado) no influye en el contenido de mercurio.
González Estecha ha explicado que “el contenido de mercurio de las latas de atún no depende del líquido de cobertura (aceite, natural, escabeche) sino que difiere según varios factores como la especie del pescado, tamaño u origen”.
Con todo ello, la coordinadora del grupo ha indicado que “es imprescindible conocer las concentraciones reales de mercurio de los pescados y mariscos (incluyendo latas) que se consumen habitualmente en España para poder aconsejar a la población, ya que la cantidad consumida de un pescado puede influir más en la carga corporal de un individuo, que el hecho de que un pescado supere o no un límite legal. En este sentido también hay que señalar que una dosis elevada puntual de MeHg puede ser más perjudicial para el sistema nervioso en desarrollo que una dosis baja crónica”.
Según recogen los documentos elaborados, existen componentes que modulan la toxicidad del MeHg, como las frutas, verduras y la fibra, que parecen disminuir la concentración de MeHg en el organismo. También es el caso de los ácidos grasos poliinsaturados que se encuentran en el pescado y en otros productos de la dieta. “Su ingesta es importante durante el desarrollo fetal y neurológico de los niños expuestos a MeHg, y se ha sugerido que la ingesta de ácidos grasos de cadena larga poliinstaurados previenen o mitigan la toxicidad del MeHg en general, y los efectos neurológicos y cardiovasculares en particular”, asegura la experta.
Además, el selenio ha recibido una gran atención como potencial protector de la toxicidad del metilmercurio en poblaciones consumidoras de pescado. El estatus de selenio se mide en suero o plasma y conviene recordar que es un elemento esencial pero también puede ser tóxico, con un rango sin efectos adversos muy estrecho.
González Estecha también ha señalado que “se ha observado in vitro que alimentos ricos en fitoquímicos como el té verde, el té negro y la proteína de soja, reducen la bioaccesibilidad del mercurio cuando se ingieren simultáneamente con pescado”.
Descubren un mecanismo a través del cual el resveratrol genera beneficios para la salud – DiarioMedico.com
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