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Calcium supplements, commonly taken by older people for osteoporosis, are associated with an increased risk of a heart attack, finds a study published online in the British Medical Journal.
The results suggest that a reassessment of the role of calcium supplements in osteoporosis management is needed.
Calcium supplements are commonly prescribed for skeletal health, but a recent trial suggested they might increase rates of heart attack (myocardial infarction) and cardiovascular events in healthy older women.
To further investigate this important issue, an international team of researchers analysed the results of 11 randomised controlled trials of calcium supplements (without co-administered vitamin D) involving 12,000 patients.
Differences in study design and quality were taken into account to minimise bias.
They found that calcium supplements were associated with about a 30% increased risk of heart attack and smaller, non-significant, increases in the risk of stroke and mortality.
The findings were consistent across trials and were independent of age, sex, and type of supplement.
Although the increase in risk is modest, the widespread use of calcium supplements means that even a small increase might translate into a large burden of disease in the population, warn the authors.
Previous studies have found no increased cardiovascular risks with higher dietary calcium intake, suggesting that the risks are restricted to supplements.
Given the modest benefits of calcium supplements on bone density and fracture prevention, a reassessment of the role of calcium supplements in osteoporosis management is warranted, they conclude.
An accompanying editorial by Professor John Cleland and colleagues suggests that, while uncertainty exists about whether the increase in heart attack and stroke is real, there are also doubts about the efficacy of calcium supplements in reducing fractures. On the basis of the limited evidence available, patients with osteoporosis should generally not be treated with calcium supplements, either alone or combined with vitamin D, unless they are also receiving an effective treatment for osteoporosis for a recognised indication. They also believe that research on whether such supplements are needed as an adjunct to effective agents is urgently required
Saturday, July 31, 2010
Thursday, July 29, 2010
Western diet link to ADHD
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A new study from Perth's Telethon Institute for Child Health Research shows an association between ADHD and a 'Western-style' diet in adolescents.
The research findings have just been published online in the international Journal of Attention Disorders.
Leader of Nutrition studies at the Institute, Associate Professor Wendy Oddy, said the study examined the dietary patterns of 1800 adolescents from the long-term Raine Study and classified diets into 'Healthy' or 'Western' patterns.
“We found a diet high in the Western pattern of foods was associated with more than double the risk of having an ADHD diagnosis compared with a diet low in the Western pattern, after adjusting for numerous other social and family influences,” Dr Oddy said.
“We looked at the dietary patterns amongst the adolescents and compared the diet information against whether or not the adolescent had received a diagnosis of ADHD by the age of 14 years. In our study, 115 adolescents had been diagnosed with ADHD, 91 boys and 24 girls.”
A “healthy” pattern is a diet high in fresh fruit and vegetables, whole grains and fish. It tends to be higher in omega-3 fatty acids, folate and fibre. A “Western” pattern is a diet with a trend towards takeaway foods, confectionary, processed, fried and refined foods. These diets tend to be higher in total fat, saturated fat, refined sugar and sodium.
“When we looked at specific foods, having an ADHD diagnosis was associated with a diet high in takeaway foods, processed meats, red meat, high fat dairy products and confectionary,” Dr Oddy said.
“We suggest that a Western dietary pattern may indicate the adolescent has a less optimal fatty acid profile, whereas a diet higher in omega-3 fatty acids is thought to hold benefits for mental health and optimal brain function.
“It also may be that the Western dietary pattern doesn't provide enough essential micronutrients that are needed for brain function, particularly attention and concentration, or that a Western diet might contain more colours, flavours and additives that have been linked to an increase in ADHD symptoms. It may also be that impulsivity, which is a characteristic of ADHD, leads to poor dietary choices such as quick snacks when hungry.”
Dr Oddy said that whilst this study suggests that diet may be implicated in ADHD, more research is needed to determine the nature of the relationship.
“This is a cross-sectional study so we cannot be sure whether a poor diet leads to ADHD or whether ADHD leads to poor dietary choices and cravings,” Dr Oddy said.
ADHD is the most commonly diagnosed childhood mental health disorder and has a prevalence of approximately 5%. ADHD is known to be more common in boys.
About the Raine Study
The Raine Study is jointly conducted by the Telethon Institute for Child Health Research and The School of Women's and Infant's Health at the University of Western Australia. The study started in 1989, when 2900 pregnant women were recruited into a research study at King Edward Memorial Hospital to examine ultrasound imaging. The mothers were assessed during pregnancy and information was collected on the mother and the father, for example diet, exercise, work, health, etc. After the children were born, they were assessed at birth, at one year, then two, three and five years of age. Further follow-ups of the cohort have been conducted at eight, ten, fourteen, seventeen and now twenty years of age.
Find out more at www.rainestudy.org.au
A new study from Perth's Telethon Institute for Child Health Research shows an association between ADHD and a 'Western-style' diet in adolescents.
The research findings have just been published online in the international Journal of Attention Disorders.
Leader of Nutrition studies at the Institute, Associate Professor Wendy Oddy, said the study examined the dietary patterns of 1800 adolescents from the long-term Raine Study and classified diets into 'Healthy' or 'Western' patterns.
“We found a diet high in the Western pattern of foods was associated with more than double the risk of having an ADHD diagnosis compared with a diet low in the Western pattern, after adjusting for numerous other social and family influences,” Dr Oddy said.
“We looked at the dietary patterns amongst the adolescents and compared the diet information against whether or not the adolescent had received a diagnosis of ADHD by the age of 14 years. In our study, 115 adolescents had been diagnosed with ADHD, 91 boys and 24 girls.”
A “healthy” pattern is a diet high in fresh fruit and vegetables, whole grains and fish. It tends to be higher in omega-3 fatty acids, folate and fibre. A “Western” pattern is a diet with a trend towards takeaway foods, confectionary, processed, fried and refined foods. These diets tend to be higher in total fat, saturated fat, refined sugar and sodium.
“When we looked at specific foods, having an ADHD diagnosis was associated with a diet high in takeaway foods, processed meats, red meat, high fat dairy products and confectionary,” Dr Oddy said.
“We suggest that a Western dietary pattern may indicate the adolescent has a less optimal fatty acid profile, whereas a diet higher in omega-3 fatty acids is thought to hold benefits for mental health and optimal brain function.
“It also may be that the Western dietary pattern doesn't provide enough essential micronutrients that are needed for brain function, particularly attention and concentration, or that a Western diet might contain more colours, flavours and additives that have been linked to an increase in ADHD symptoms. It may also be that impulsivity, which is a characteristic of ADHD, leads to poor dietary choices such as quick snacks when hungry.”
Dr Oddy said that whilst this study suggests that diet may be implicated in ADHD, more research is needed to determine the nature of the relationship.
“This is a cross-sectional study so we cannot be sure whether a poor diet leads to ADHD or whether ADHD leads to poor dietary choices and cravings,” Dr Oddy said.
ADHD is the most commonly diagnosed childhood mental health disorder and has a prevalence of approximately 5%. ADHD is known to be more common in boys.
About the Raine Study
The Raine Study is jointly conducted by the Telethon Institute for Child Health Research and The School of Women's and Infant's Health at the University of Western Australia. The study started in 1989, when 2900 pregnant women were recruited into a research study at King Edward Memorial Hospital to examine ultrasound imaging. The mothers were assessed during pregnancy and information was collected on the mother and the father, for example diet, exercise, work, health, etc. After the children were born, they were assessed at birth, at one year, then two, three and five years of age. Further follow-ups of the cohort have been conducted at eight, ten, fourteen, seventeen and now twenty years of age.
Find out more at www.rainestudy.org.au
Resveratrol Shown to Suppress Inflammation, Free Radicals, in Humans
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Resveratrol, a popular plant extract shown to prolong life in yeast and lower animals due to its anti-inflammatory and antioxidant properties, appears also to suppress inflammation in humans, based on results from the first prospective human trial of the extract conducted by University at Buffalo endocrinologists.
Results of the study appear as a rapid electronic publication on the Journal of Clinical Endocrinology & Metabolism website and will be published in an upcoming print issue of the journal.
The paper also has been selected for inclusion in Translational Research in Endocrinology & Metabolism, a new online anthology that highlights the latest clinical applications of cutting-edge research from the journals of the Endocrine Society.
Resveratrol is a compound produced naturally by several plants when under attack by pathogens such as bacteria or fungi, and is found in the skin of red grapes and red wine. It also is produced by chemical synthesis derived primarily from Japanese knotweed and is sold as a nutritional supplement.
Husam Ghanim, PhD, UB research assistant professor of medicine and first author on the study, notes that resveratrol has been shown to prolong life and to reduce the rate of aging in yeast, roundworms and fruit flies, actions thought to be affected by increased expression of a particular gene associated with longevity.
The compound also is thought to play a role in insulin resistance as well, a condition related to oxidative stress, which has a significant detrimental effect on overall health.
"Since there are no data demonstrating the effect of resveratrol on oxidative and inflammatory stress in humans," says Paresh Dandona, MD, PhD, UB distinguished professor of medicine and senior author on the study, "we decided to determine if the compound reduces the level of oxidative and inflammatory stress in humans.
"Several of the key mediators of insulin resistance also are pro-inflammatory, so we investigated the effect of resveratrol on their expression as well."
The study was conducted at Kaleida Health's Diabetes-Endocrinology Center of Western New York, which Dandona directs.
A nutritional supplement containing 40 milligrams of resveratrol was used as the active product. Twenty participants were randomized into two groups of 10: one group received the supplement, while the other group received an identical pill containing no active ingredient. Participants took the pill once a day for six weeks. Fasting blood samples were collected as the start of the trial and at weeks one, three and six.
Results showed that resveratrol suppressed the generation of free radicals, or reactive oxygen species, unstable molecules known to cause oxidative stress and release proinflammatory factors into the blood stream, resulting in damage to the blood vessel lining.
Blood samples from persons taking resveratrol also showed suppression of the inflammatory protein tumor necrosis factor (TNF) and other similar compounds that increase inflammation in blood vessels and interfere with insulin action, causing insulin resistance and the risk of developing diabetes.
These inflammatory factors, in the long term, have an impact on the development of type 2 diabetes, aging, heart disease and stroke, noted Dandona.
Blood samples from the participants who received the placebo showed no change in these pro-inflammatory markers.
While these results are promising, Dandona added a caveat: The study didn't eliminate the possibility that something in the extract other than resveratrol was responsible for the anti-inflammatory effects.
"The product we used has only 20 percent resveratrol, so it is possible that something else in the preparation is responsible for the positive effects. These agents could be even more potent than resveratrol. Purer preparations now are available and we intend to test those."
Resveratrol, a popular plant extract shown to prolong life in yeast and lower animals due to its anti-inflammatory and antioxidant properties, appears also to suppress inflammation in humans, based on results from the first prospective human trial of the extract conducted by University at Buffalo endocrinologists.
Results of the study appear as a rapid electronic publication on the Journal of Clinical Endocrinology & Metabolism website and will be published in an upcoming print issue of the journal.
The paper also has been selected for inclusion in Translational Research in Endocrinology & Metabolism, a new online anthology that highlights the latest clinical applications of cutting-edge research from the journals of the Endocrine Society.
Resveratrol is a compound produced naturally by several plants when under attack by pathogens such as bacteria or fungi, and is found in the skin of red grapes and red wine. It also is produced by chemical synthesis derived primarily from Japanese knotweed and is sold as a nutritional supplement.
Husam Ghanim, PhD, UB research assistant professor of medicine and first author on the study, notes that resveratrol has been shown to prolong life and to reduce the rate of aging in yeast, roundworms and fruit flies, actions thought to be affected by increased expression of a particular gene associated with longevity.
The compound also is thought to play a role in insulin resistance as well, a condition related to oxidative stress, which has a significant detrimental effect on overall health.
"Since there are no data demonstrating the effect of resveratrol on oxidative and inflammatory stress in humans," says Paresh Dandona, MD, PhD, UB distinguished professor of medicine and senior author on the study, "we decided to determine if the compound reduces the level of oxidative and inflammatory stress in humans.
"Several of the key mediators of insulin resistance also are pro-inflammatory, so we investigated the effect of resveratrol on their expression as well."
The study was conducted at Kaleida Health's Diabetes-Endocrinology Center of Western New York, which Dandona directs.
A nutritional supplement containing 40 milligrams of resveratrol was used as the active product. Twenty participants were randomized into two groups of 10: one group received the supplement, while the other group received an identical pill containing no active ingredient. Participants took the pill once a day for six weeks. Fasting blood samples were collected as the start of the trial and at weeks one, three and six.
Results showed that resveratrol suppressed the generation of free radicals, or reactive oxygen species, unstable molecules known to cause oxidative stress and release proinflammatory factors into the blood stream, resulting in damage to the blood vessel lining.
Blood samples from persons taking resveratrol also showed suppression of the inflammatory protein tumor necrosis factor (TNF) and other similar compounds that increase inflammation in blood vessels and interfere with insulin action, causing insulin resistance and the risk of developing diabetes.
These inflammatory factors, in the long term, have an impact on the development of type 2 diabetes, aging, heart disease and stroke, noted Dandona.
Blood samples from the participants who received the placebo showed no change in these pro-inflammatory markers.
While these results are promising, Dandona added a caveat: The study didn't eliminate the possibility that something in the extract other than resveratrol was responsible for the anti-inflammatory effects.
"The product we used has only 20 percent resveratrol, so it is possible that something else in the preparation is responsible for the positive effects. These agents could be even more potent than resveratrol. Purer preparations now are available and we intend to test those."
CPR Without Mouth-to-Mouth Rescue Breathing May Be Better for Many Victims of Cardiac Arrest; Chest Compressions Alone Save More Lives
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A leading expert in cardiopulmonary resuscitation says two new studies from U.S. and European researchers support the case for dropping mouth-to-mouth, or rescue breathing by bystanders and using "hands-only" chest compressions during the life-saving practice, better known as CPR.
The findings, the expert says, concur with the latest science advisory statement from the American Heart Association (AHA), published in 2008, recommending hands-only (or compression-only) CPR by bystanders who are not adequately trained or who feel uncomfortable with performing rescue breathing on other adults who collapse from sudden cardiac arrest.
In an editorial accompanying the studies, to be published in the New England Journal of Medicine online July 29, cardiologist Myron "Mike" Weisfeldt, M.D., physician in chief at The Johns Hopkins Hospital and director of the Department of Medicine at Hopkins' School of Medicine, says "less may be better" in CPR, calling the findings straightforward, practical and potentially life-saving.
The two studies were conducted between 2004 and 2009 on more than 3,000 men and women who needed CPR. Among their key findings are that survival rates were similar for adults who received their CPR from bystanders randomly assigned to provide only chest compressions and those who were instructed to do standard CPR with rescue breathing. All bystanders involved in the studies were instructed by phone on which CPR method to use by 911 telephone dispatchers. One study showed survival rates after one month of 8.7 percent and 7 percent, respectively, while the other showed survival rates at time of hospital discharge of 12.5 percent and 11 percent. The researchers say the numbers were statistically the same.
"It is very important to understand that the patients in this study were adults and that for most children who suffer cardiac arrest, such as drowning victims, we must do rescue breathing," says Weisfeldt, a past president of the AHA (1989-1990).
He also notes that there are adults with breathing-related causes of sudden death where rescue breathing should be performed, including patients with sudden, acute heart failure, severe chronic lung disease, or acute asthma, and cardiac arrest.
However, says Weisfeldt, "for people who are not well trained or who are looking for a simple way to help save a life, chest compressions only, at least until the emergency care unit arrives, can be life saving, even without rescue breathing."
Weisfeldt says the studies' results could lead to stronger national guidelines on how bystanders should perform CPR. An update is expected to be announced in November in Chicago at an AHA annual meeting. Guidelines, he says, will likely recommend a steady 100 chest compressions per minute with less emphasis on rescue breathing.
Weisfeldt points out that both recent studies and previous animal studies had shown that hands-only CPR worked best for certain types of cardiac arrest, mostly instances resulting from an abnormal heart rhythm (and requiring defibrillation).
CPR has been in practice in the United States since 1960, when Johns Hopkins researchers William Kouwenhoven, Ph.D., Guy Knickerbocker, Ph.D., and James Jude, M.D., published the first data on the benefits of what was then called "cardiac massage."
Weisfeldt says further research is needed to see if a combination of CPR with rescue breathing is better at saving lives in certain kinds of cardiac arrest, and to see how and if the public can be trained to recognize and distinguish between types of heart attack.
A third of the estimated 300,000 Americans each year whose heart suddenly stops beating outside of a hospital receive CPR to keep blood and oxygen flowing to the body's vital organs in the torso until emergency services personnel arrive. CPR performed by good Samaritans is known to nearly double the survival chances of people who suffer sudden cardiac arrest.
A leading expert in cardiopulmonary resuscitation says two new studies from U.S. and European researchers support the case for dropping mouth-to-mouth, or rescue breathing by bystanders and using "hands-only" chest compressions during the life-saving practice, better known as CPR.
The findings, the expert says, concur with the latest science advisory statement from the American Heart Association (AHA), published in 2008, recommending hands-only (or compression-only) CPR by bystanders who are not adequately trained or who feel uncomfortable with performing rescue breathing on other adults who collapse from sudden cardiac arrest.
In an editorial accompanying the studies, to be published in the New England Journal of Medicine online July 29, cardiologist Myron "Mike" Weisfeldt, M.D., physician in chief at The Johns Hopkins Hospital and director of the Department of Medicine at Hopkins' School of Medicine, says "less may be better" in CPR, calling the findings straightforward, practical and potentially life-saving.
The two studies were conducted between 2004 and 2009 on more than 3,000 men and women who needed CPR. Among their key findings are that survival rates were similar for adults who received their CPR from bystanders randomly assigned to provide only chest compressions and those who were instructed to do standard CPR with rescue breathing. All bystanders involved in the studies were instructed by phone on which CPR method to use by 911 telephone dispatchers. One study showed survival rates after one month of 8.7 percent and 7 percent, respectively, while the other showed survival rates at time of hospital discharge of 12.5 percent and 11 percent. The researchers say the numbers were statistically the same.
"It is very important to understand that the patients in this study were adults and that for most children who suffer cardiac arrest, such as drowning victims, we must do rescue breathing," says Weisfeldt, a past president of the AHA (1989-1990).
He also notes that there are adults with breathing-related causes of sudden death where rescue breathing should be performed, including patients with sudden, acute heart failure, severe chronic lung disease, or acute asthma, and cardiac arrest.
However, says Weisfeldt, "for people who are not well trained or who are looking for a simple way to help save a life, chest compressions only, at least until the emergency care unit arrives, can be life saving, even without rescue breathing."
Weisfeldt says the studies' results could lead to stronger national guidelines on how bystanders should perform CPR. An update is expected to be announced in November in Chicago at an AHA annual meeting. Guidelines, he says, will likely recommend a steady 100 chest compressions per minute with less emphasis on rescue breathing.
Weisfeldt points out that both recent studies and previous animal studies had shown that hands-only CPR worked best for certain types of cardiac arrest, mostly instances resulting from an abnormal heart rhythm (and requiring defibrillation).
CPR has been in practice in the United States since 1960, when Johns Hopkins researchers William Kouwenhoven, Ph.D., Guy Knickerbocker, Ph.D., and James Jude, M.D., published the first data on the benefits of what was then called "cardiac massage."
Weisfeldt says further research is needed to see if a combination of CPR with rescue breathing is better at saving lives in certain kinds of cardiac arrest, and to see how and if the public can be trained to recognize and distinguish between types of heart attack.
A third of the estimated 300,000 Americans each year whose heart suddenly stops beating outside of a hospital receive CPR to keep blood and oxygen flowing to the body's vital organs in the torso until emergency services personnel arrive. CPR performed by good Samaritans is known to nearly double the survival chances of people who suffer sudden cardiac arrest.
Stroke risk temporarily increases for an hour after drinking alcohol
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Call it the not-so-happy hour. The risk of stroke appears to double in the hour after consuming just one drink — be it wine, beer or hard liquor — according to a small multi-center study reported in Stroke: Journal of the American Heart Association.
“The impact of alcohol on your risk of ischemic stroke appears to depend on how much and how often you drink,” said Murray A. Mittleman, M.D., Dr.P.H., senior author of the Stroke Onset Study (SOS) and director of the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center in the Harvard Medical School in Boston, Mass.
Prior to the SOS, researchers didn’t know if alcohol consumption had an immediate impact on ischemic stroke (caused by a blood clot in a vessel in or leading to the brain), although modest alcohol use (less than two drinks per day) may potentially lower risk in the long term.
Researchers interviewed 390 ischemic stroke patients (209 men, 181 women) about three days after their stroke regarding many aspects of their lives. Patients were excluded if the stroke seriously impaired their ability to speak or if they weren’t well enough to participate. Fourteen patients had consumed alcohol within one hour of stroke onset.
Compared with times when alcohol wasn’t being used, the relative risk of stroke after alcohol consumption was:
* 2.3 times higher in the first hour;
* 1.6 times higher in the second hour; and
* 30 percent lower than baseline after 24 hours.
The patterns remained the same whether participants had consumed wine, beer or distilled spirits. When the researchers eliminated patients who had been exposed to other potential triggers (such as exercising vigorously or drinking a caffeinated beverage) just prior to their strokes, the alcohol connection didn’t change. Only one participant had consumed more than two drinks in the hour preceding the stroke, and removing that data didn’t alter the pattern.
“The evidence on heavy drinking is consistent: Both in the long and short term it raises stroke risk,” Mittleman said. “But we’re finding it’s more complicated with light to moderate drinking. It is possible that the transiently increased stroke risk from moderate alcohol consumption may be outweighed by the longer term health benefits.”
Just after drinking, blood pressure rises and blood platelets become stickier, which may increase the possibility of a clot forming. However, consistent use of small amounts of alcohol is associated with beneficial changes in blood lipids and more flexible blood vessels, which may reduce risk overall.
“At this point we don’t have enough evidence to say that people who don’t drink should start, or that people who drink small amounts — on the order of one drink a day — should stop,” Mittleman said.
A more definitive answer would require a controlled study in which some people are randomly selected to consume alcohol while others don’t, he said.
The findings may not apply to patients with severe stroke.
Stroke is the No. 3 killer and a leading cause of long-term major disability in the United States, according to American Heart Association statistics.
The American Heart Association recommends that if you drink alcohol, do so in moderation. This means no more than two drinks per day for men and one drink per day for women. (A drink is one 12-ounce beer, 4 ounces of wine, 1.5 ounces of 80-proof spirits, or 1 ounce of 100-proof spirits.) High intakes can be associated with serious adverse effects and may increase alcoholism, high blood pressure, obesity, stroke, breast cancer, suicide and accidents. Consult your doctor on the benefits and risks of consuming alcohol in moderation.
Ω
Call it the not-so-happy hour. The risk of stroke appears to double in the hour after consuming just one drink — be it wine, beer or hard liquor — according to a small multi-center study reported in Stroke: Journal of the American Heart Association.
“The impact of alcohol on your risk of ischemic stroke appears to depend on how much and how often you drink,” said Murray A. Mittleman, M.D., Dr.P.H., senior author of the Stroke Onset Study (SOS) and director of the Cardiovascular Epidemiology Research Unit at Beth Israel Deaconess Medical Center in the Harvard Medical School in Boston, Mass.
Prior to the SOS, researchers didn’t know if alcohol consumption had an immediate impact on ischemic stroke (caused by a blood clot in a vessel in or leading to the brain), although modest alcohol use (less than two drinks per day) may potentially lower risk in the long term.
Researchers interviewed 390 ischemic stroke patients (209 men, 181 women) about three days after their stroke regarding many aspects of their lives. Patients were excluded if the stroke seriously impaired their ability to speak or if they weren’t well enough to participate. Fourteen patients had consumed alcohol within one hour of stroke onset.
Compared with times when alcohol wasn’t being used, the relative risk of stroke after alcohol consumption was:
* 2.3 times higher in the first hour;
* 1.6 times higher in the second hour; and
* 30 percent lower than baseline after 24 hours.
The patterns remained the same whether participants had consumed wine, beer or distilled spirits. When the researchers eliminated patients who had been exposed to other potential triggers (such as exercising vigorously or drinking a caffeinated beverage) just prior to their strokes, the alcohol connection didn’t change. Only one participant had consumed more than two drinks in the hour preceding the stroke, and removing that data didn’t alter the pattern.
“The evidence on heavy drinking is consistent: Both in the long and short term it raises stroke risk,” Mittleman said. “But we’re finding it’s more complicated with light to moderate drinking. It is possible that the transiently increased stroke risk from moderate alcohol consumption may be outweighed by the longer term health benefits.”
Just after drinking, blood pressure rises and blood platelets become stickier, which may increase the possibility of a clot forming. However, consistent use of small amounts of alcohol is associated with beneficial changes in blood lipids and more flexible blood vessels, which may reduce risk overall.
“At this point we don’t have enough evidence to say that people who don’t drink should start, or that people who drink small amounts — on the order of one drink a day — should stop,” Mittleman said.
A more definitive answer would require a controlled study in which some people are randomly selected to consume alcohol while others don’t, he said.
The findings may not apply to patients with severe stroke.
Stroke is the No. 3 killer and a leading cause of long-term major disability in the United States, according to American Heart Association statistics.
The American Heart Association recommends that if you drink alcohol, do so in moderation. This means no more than two drinks per day for men and one drink per day for women. (A drink is one 12-ounce beer, 4 ounces of wine, 1.5 ounces of 80-proof spirits, or 1 ounce of 100-proof spirits.) High intakes can be associated with serious adverse effects and may increase alcoholism, high blood pressure, obesity, stroke, breast cancer, suicide and accidents. Consult your doctor on the benefits and risks of consuming alcohol in moderation.
Ω
Wednesday, July 28, 2010
Nutrients For Eye Health
Lutein and zeaxanthin are important nutrients found in spinach, corn, broccoli and eggs. Many studies have shown that lutein and zeaxanthin reduce the risk of chronic eye diseases, including age-related macular degeneration (AMD) and cataracts. AMD is the leading cause of blindness in people over age 55 in the Western world and the incidence is expected to triple by 2025.
Beyond reducing the risk of developing eye disease, separate studies have shown that lutein and zeaxanthin improve visual performance in AMD patients, cataract patients and individuals with good health.
Cataracts
The primary function of the crystalline lens (or natural lens in the eye) is to collect and focus light on the retina. To properly provide this function throughout life, the lens must remain clear. Oxidation of the lens is a major cause of cataracts, which cloud the lens. As antioxidant nutrients neutralize free radicals (unstable molecules) associated with oxidative stress and retinal damage, lutein and zeaxanthin likely play a role in cataract prevention. In fact, a recent study demonstrated that higher dietary intakes of lutein and zeaxanthin and vitamin E was associated with a significantly decreased risk of cataract formation.
AMD
Much evidence supports the role of lutein and zeaxanthin in reducing the risk of AMD. Although there is no recommended daily intake for lutein and zeaxanthin, most recent studies show a health benefit for lutein supplementation at 10 mg/day and leaxanthin supplementation at 2 mg/day. In fact, The National Eye Institute presently is conducting a second large human clinical trial, Age-Related Eye Disease Study (AREDS2), to confirm whether supplements containing 10 mg a day of lutein and 2 mg of zeaxanthin per day, affect the risk of developing AMD.
Beyond reducing the risk of developing eye disease, separate studies have shown that lutein and zeaxanthin improve visual performance in AMD patients, cataract patients and individuals with good health.
Cataracts
The primary function of the crystalline lens (or natural lens in the eye) is to collect and focus light on the retina. To properly provide this function throughout life, the lens must remain clear. Oxidation of the lens is a major cause of cataracts, which cloud the lens. As antioxidant nutrients neutralize free radicals (unstable molecules) associated with oxidative stress and retinal damage, lutein and zeaxanthin likely play a role in cataract prevention. In fact, a recent study demonstrated that higher dietary intakes of lutein and zeaxanthin and vitamin E was associated with a significantly decreased risk of cataract formation.
AMD
Much evidence supports the role of lutein and zeaxanthin in reducing the risk of AMD. Although there is no recommended daily intake for lutein and zeaxanthin, most recent studies show a health benefit for lutein supplementation at 10 mg/day and leaxanthin supplementation at 2 mg/day. In fact, The National Eye Institute presently is conducting a second large human clinical trial, Age-Related Eye Disease Study (AREDS2), to confirm whether supplements containing 10 mg a day of lutein and 2 mg of zeaxanthin per day, affect the risk of developing AMD.
Monday, July 26, 2010
Niacin = Good: Flushing, Bad
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Cholesterol influences the health of our hearts and blood vessels. Conventional treatment attempts to reduce the level of "bad" cholesterol, LDL cholesterol, in the blood plasma. The opposite approach, which involves increasing the concentration of "good" HDL cholesterol using nicotinic acid, has proven unpopular among patients up to now. The reason for this is that treatment with nicotinic acid (niacin) has an unpleasant but harmless side-effect: the drug makes patients turn quite red in the face.
Scientists at the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now discovered the mechanism behind this effect, which is known as flushing. This will enable the development of flush inhibitors and thereby the more effective prevention of cardiovascular diseases. (Journal of Clinical Investigation, online version: July 26, 2010)
In addition to a healthy lifestyle, the treatment of lipid metabolic disorders is one of the important measures used in the prevention of cardio-vascular disease. Cholesterol is the key molecule here and LDL cholesterol is the type of cholesterol most widely discussed in this context. This "bad" cholesterol is one of the most important risk factors for the emergence of cardio-vascular diseases. The higher the blood-plasma concentration of LDL cholesterol, the higher an individual's risk of suffering cardiac arrest, stroke or peripheral vascular disease. The opposite applies to the "good" HDL cholesterol: in other words, the higher an individual's level of HDL cholesterol, the lower his or her risk of contracting these diseases. For this reason, the strategy of increasing HDL plasma concentration through medication has become more prevalent of late. The drug on which most hopes are pinned here is nicotinic acid.
"The main problem with treatment using nicotinic acid – which has nothing to do with the nicotine in tobacco, by the way – is flushing," says Stefan Offermanns, Director of the Department of Pharmacology at the Max Planck Institute for Heart and Lung Research. "Just a short time after taking nicotinic acid, the patient experiences strong flushing of the face and upper body for up to one and a half hours. This is caused by the dilation of blood vessels in the skin." The flushing symptoms, which are combined with a strong sensation of heat and burning, are comparable with those of sunburn, but otherwise completely harmless. However, patients often abandon the treatment on account of these symptoms.
This flushing phenomenon is a typical pharmacological problem whereby desired and undesired effects arise simultaneously. Hence, the Bad Nauheim scientists set themselves the objective of understanding the mechanisms behind the desired and, in particular, undesired effects of nicotinic acid. The results of this study are to be published in the August issue of the Journal of Clinical Investigation.
Offermanns and his colleagues had already succeeded in identifying a specific receptor for nicotinic acid that conveys the desired effects of nicotinic acid. Tests on mice, in which the gene for this receptor had been deactivated, showed, however, that the receptor is also responsible for the nicotinic-acid-induced flushing reaction. "We have now succeeded in demonstrating that the receptor exists both in the main cells of the top layer of the skin or epidermis, which are called keratinocytes, and the immune cells, known as Langerhans cells, also found in the epidermis," reports Offermanns. By studying genetically modified mouse strains in which the receptor in either the Langerhans cells or keratinocytes is blocked, the Max Planck researchers were able to show that the first phase of the flushing reaction is triggered by the activation of Langerhans cells. In contrast, the second and longer phase results from the activation of the keratinocytes. In both phases, different prostaglandins are formed through the activation of the nicotinic acid receptor. "The flushing phenomenon can be prevented by inhibiting prostaglandin formation or blocking the prostaglandin receptors in the skin, while the desired effects of the nicotinic acid on lipid metabolism remain unaffected."
Offermanns firmly believes that these findings provide a basis for the development of innovative methods for the inhibition of the undesired flushing reaction caused by nicotinic acid treatment. Several pharmaceutical companies have already started work on the development of novel "flush inhibitors" which would reduce prostaglandin formation or block the prostaglandin effect. The future administration of these inhibitors in combination with nicotinic acid would eliminate the unpleasant side effects, which have been responsible for the low level of acceptance of the drug among patients to date.
Cholesterol influences the health of our hearts and blood vessels. Conventional treatment attempts to reduce the level of "bad" cholesterol, LDL cholesterol, in the blood plasma. The opposite approach, which involves increasing the concentration of "good" HDL cholesterol using nicotinic acid, has proven unpopular among patients up to now. The reason for this is that treatment with nicotinic acid (niacin) has an unpleasant but harmless side-effect: the drug makes patients turn quite red in the face.
Scientists at the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now discovered the mechanism behind this effect, which is known as flushing. This will enable the development of flush inhibitors and thereby the more effective prevention of cardiovascular diseases. (Journal of Clinical Investigation, online version: July 26, 2010)
In addition to a healthy lifestyle, the treatment of lipid metabolic disorders is one of the important measures used in the prevention of cardio-vascular disease. Cholesterol is the key molecule here and LDL cholesterol is the type of cholesterol most widely discussed in this context. This "bad" cholesterol is one of the most important risk factors for the emergence of cardio-vascular diseases. The higher the blood-plasma concentration of LDL cholesterol, the higher an individual's risk of suffering cardiac arrest, stroke or peripheral vascular disease. The opposite applies to the "good" HDL cholesterol: in other words, the higher an individual's level of HDL cholesterol, the lower his or her risk of contracting these diseases. For this reason, the strategy of increasing HDL plasma concentration through medication has become more prevalent of late. The drug on which most hopes are pinned here is nicotinic acid.
"The main problem with treatment using nicotinic acid – which has nothing to do with the nicotine in tobacco, by the way – is flushing," says Stefan Offermanns, Director of the Department of Pharmacology at the Max Planck Institute for Heart and Lung Research. "Just a short time after taking nicotinic acid, the patient experiences strong flushing of the face and upper body for up to one and a half hours. This is caused by the dilation of blood vessels in the skin." The flushing symptoms, which are combined with a strong sensation of heat and burning, are comparable with those of sunburn, but otherwise completely harmless. However, patients often abandon the treatment on account of these symptoms.
This flushing phenomenon is a typical pharmacological problem whereby desired and undesired effects arise simultaneously. Hence, the Bad Nauheim scientists set themselves the objective of understanding the mechanisms behind the desired and, in particular, undesired effects of nicotinic acid. The results of this study are to be published in the August issue of the Journal of Clinical Investigation.
Offermanns and his colleagues had already succeeded in identifying a specific receptor for nicotinic acid that conveys the desired effects of nicotinic acid. Tests on mice, in which the gene for this receptor had been deactivated, showed, however, that the receptor is also responsible for the nicotinic-acid-induced flushing reaction. "We have now succeeded in demonstrating that the receptor exists both in the main cells of the top layer of the skin or epidermis, which are called keratinocytes, and the immune cells, known as Langerhans cells, also found in the epidermis," reports Offermanns. By studying genetically modified mouse strains in which the receptor in either the Langerhans cells or keratinocytes is blocked, the Max Planck researchers were able to show that the first phase of the flushing reaction is triggered by the activation of Langerhans cells. In contrast, the second and longer phase results from the activation of the keratinocytes. In both phases, different prostaglandins are formed through the activation of the nicotinic acid receptor. "The flushing phenomenon can be prevented by inhibiting prostaglandin formation or blocking the prostaglandin receptors in the skin, while the desired effects of the nicotinic acid on lipid metabolism remain unaffected."
Offermanns firmly believes that these findings provide a basis for the development of innovative methods for the inhibition of the undesired flushing reaction caused by nicotinic acid treatment. Several pharmaceutical companies have already started work on the development of novel "flush inhibitors" which would reduce prostaglandin formation or block the prostaglandin effect. The future administration of these inhibitors in combination with nicotinic acid would eliminate the unpleasant side effects, which have been responsible for the low level of acceptance of the drug among patients to date.
Friday, July 23, 2010
Raising HDL Still Beneficial
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The European Society of Cardiology (ESC) is concerned that interpretations of a paper about cholesterol, published in the Lancet (1), could act to deter ongoing research efforts into developing new therapeutic strategies to increase high density lipoprotein (HDL) cholesterol. Caution, the ESC experts advise, should be displayed in the interpretation of the results.
In the Lancet study, Paul Ridker and colleagues, from Brigham and Women’s Hospital (Boston, MA, USA), undertook a retrospective post-hoc analysis of the JUPITER trial. The results show that if a normal, healthy individual has level of low density lipoprotein (LDL), known as “bad cholesterol”, substantially lowered with a potent statin, then the level of HDL “good cholesterol” in that person no longer bears any relation to the remaining cardiovascular risk.
The original JUPITER trial (2) was designed to answer the critical question of whether rosuvastatin prevents cardiovascular disease among healthy people with normal LDL cholesterol levels, but increased levels of high-sensitivity C-reactive protein, a marker of chronic low level inflammation, considered a new risk factor for cardiovascular events.
The current Lancet study showed that when 17,802 subjects were divided into quartiles of HDL cholesterol concentrations, HDL cholesterol concentrations were inversely related to vascular risk at the end of study for individuals randomised to placebo, with the top quartile having a 46% reduced risk compared to the bottom quartile (p=0.0039). In contrast, however, among those subjects given active treatment with rosuvastatin, vascular risk was calculated to be similar for subjects in both the top and bottom HDL quartiles (p=0.82)
“Although measurement of HDL–cholesterol concentration is useful as part of initial cardiovascular risk assessment, HDL-cholesterol concentrations are not predictive of residual vascular risk among patients treated with potent statin therapy who attain very low concentrations of LDL cholesterol,” the authors of the study conclude.
ESC spokesperson Professor Dan Atar, from Oslo University Hospital, Norway, believes there are dangers in interpreting the study as showing that raising HDL levels produces no beneficial cardiovascular effects. “It’s a matter of statistics. If you’re looking at populations with a very low incidence of cardiovascular events, and then with an intervention of any kind you reduce the risk of events even further, it’s logical that you’ll washout the influence of any other effect. These patients already have achieved such low levels of LDL that no other marker will prevail as a predictor of the few remaining events.”
He added that he had concerns that readers of the paper might not appreciate that more data was needed before the scientific community could make a qualified decision about whether raising HDL levels was beneficial or not. “With subgroup analyses, such as the one presented here, you just can’t make such judgements,” he said.
In fact, previous studies, such as the Helsinki Heart Study (3) and the VA-HIT Study (4), have been successful in raising HDL and reducing cardiovascular events, using gemfibrozil, however this agent also concomitantly lowers LDL. Additionally, the drug nicacin has been shown to be effective at elevating HDL and reducing cardiovascular morbidity in the Coronary Drug Project Study (5), but this strategy could not easily be implemented into clinical practice due to unpleasant side effects, notably flushing. It is hoped that laropiprant, a novel flushing pathway inhibitor, will overcome this limitation.
A clearer indication of the benefit of raising HDL, Atar added, will come from the ongoing phase III Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE), which has enrolled 25,000 patients to investigate whether the combination of niacin/laropiprant can further reduce the risk for myocardial infarction, stroke and the need for revascularisation in patients already treated to lower LDL.
The European Society of Cardiology (ESC) is concerned that interpretations of a paper about cholesterol, published in the Lancet (1), could act to deter ongoing research efforts into developing new therapeutic strategies to increase high density lipoprotein (HDL) cholesterol. Caution, the ESC experts advise, should be displayed in the interpretation of the results.
In the Lancet study, Paul Ridker and colleagues, from Brigham and Women’s Hospital (Boston, MA, USA), undertook a retrospective post-hoc analysis of the JUPITER trial. The results show that if a normal, healthy individual has level of low density lipoprotein (LDL), known as “bad cholesterol”, substantially lowered with a potent statin, then the level of HDL “good cholesterol” in that person no longer bears any relation to the remaining cardiovascular risk.
The original JUPITER trial (2) was designed to answer the critical question of whether rosuvastatin prevents cardiovascular disease among healthy people with normal LDL cholesterol levels, but increased levels of high-sensitivity C-reactive protein, a marker of chronic low level inflammation, considered a new risk factor for cardiovascular events.
The current Lancet study showed that when 17,802 subjects were divided into quartiles of HDL cholesterol concentrations, HDL cholesterol concentrations were inversely related to vascular risk at the end of study for individuals randomised to placebo, with the top quartile having a 46% reduced risk compared to the bottom quartile (p=0.0039). In contrast, however, among those subjects given active treatment with rosuvastatin, vascular risk was calculated to be similar for subjects in both the top and bottom HDL quartiles (p=0.82)
“Although measurement of HDL–cholesterol concentration is useful as part of initial cardiovascular risk assessment, HDL-cholesterol concentrations are not predictive of residual vascular risk among patients treated with potent statin therapy who attain very low concentrations of LDL cholesterol,” the authors of the study conclude.
ESC spokesperson Professor Dan Atar, from Oslo University Hospital, Norway, believes there are dangers in interpreting the study as showing that raising HDL levels produces no beneficial cardiovascular effects. “It’s a matter of statistics. If you’re looking at populations with a very low incidence of cardiovascular events, and then with an intervention of any kind you reduce the risk of events even further, it’s logical that you’ll washout the influence of any other effect. These patients already have achieved such low levels of LDL that no other marker will prevail as a predictor of the few remaining events.”
He added that he had concerns that readers of the paper might not appreciate that more data was needed before the scientific community could make a qualified decision about whether raising HDL levels was beneficial or not. “With subgroup analyses, such as the one presented here, you just can’t make such judgements,” he said.
In fact, previous studies, such as the Helsinki Heart Study (3) and the VA-HIT Study (4), have been successful in raising HDL and reducing cardiovascular events, using gemfibrozil, however this agent also concomitantly lowers LDL. Additionally, the drug nicacin has been shown to be effective at elevating HDL and reducing cardiovascular morbidity in the Coronary Drug Project Study (5), but this strategy could not easily be implemented into clinical practice due to unpleasant side effects, notably flushing. It is hoped that laropiprant, a novel flushing pathway inhibitor, will overcome this limitation.
A clearer indication of the benefit of raising HDL, Atar added, will come from the ongoing phase III Heart Protection Study 2-Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE), which has enrolled 25,000 patients to investigate whether the combination of niacin/laropiprant can further reduce the risk for myocardial infarction, stroke and the need for revascularisation in patients already treated to lower LDL.
Thursday, July 22, 2010
More time spent sitting = higher risk of death
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Risk found to be independent of physical activity level
A new study from American Cancer Society researchers finds it's not just how much physical activity you get, but how much time you spend sitting that can affect your risk of death. Researchers say time spent sitting was independently associated with total mortality, regardless of physical activity level. They conclude that public health messages should promote both being physically active and reducing time spent sitting. The study appears early online in the American Journal of Epidemiology.
Increasing obesity levels in the United States are widely predicted to have major public health consequences. A growing epidemic of overweight and obesity has been attributed in part to reduced overall physical activity. And while several studies support a link between sitting time and obesity, type 2 diabetes, cardiovascular disease risk factors (11, 16, 17), and unhealthy dietary patterns in children and adults (18-20), very few studies have examined time spent sitting in relation to total mortality (21-23). Thus, public health guidelines focus largely on increasing physical activity with little or no reference to reducing time spent sitting.
To explore the association between sitting time and mortality, researchers led by Alpa Patel, Ph.D. analyzed survey responses from 123,216 individuals (53,440 men and 69,776 women) who had no history of cancer, heart attack, stroke, or emphysema/other lung disease enrolled in the American Cancer Society's Cancer Prevention II study in 1992. They examined the amount of time spent sitting and physical activity in relation to mortality between 1993 and 2006. They found that more leisure time spent sitting was associated with higher risk of mortality, particularly in women. Women who reported more than six hours per day of sitting were 37 percent more likely to die during the time period studied than those who sat fewer than 3 hours a day. Men who sat more than 6 hours a day were 18 percent more likely to die than those who sat fewer than 3 hours per day. The association remained virtually unchanged after adjusting for physical activity level. Associations were stronger for cardiovascular disease mortality than for cancer mortality.
When combined with a lack of physical activity, the association was even stronger. Women and men who both sat more and were less physically were 94% and 48% more likely, respectively, to die compared with those who reported sitting the least and being most active.
"Several factors could explain the positive association between time spent sitting and higher all-cause death rates," said Dr. Patel. "Prolonged time spent sitting, independent of physical activity, has been shown to have important metabolic consequences, and may influence things like triglycerides, high density lipoprotein, cholesterol, fasting plasma glucose, resting blood pressure, and leptin, which are biomarkers of obesity and cardiovascular and other chronic diseases."
The authors conclude that "public health messages and guidelines should be refined to include reducing time spent sitting in addition to promoting physical activity. Because a sizeable fraction of the population spends much of their time sitting, it is beneficial to encourage sedentary individuals to stand up and walk around as well as to reach optimal levels of physical activity."
Risk found to be independent of physical activity level
A new study from American Cancer Society researchers finds it's not just how much physical activity you get, but how much time you spend sitting that can affect your risk of death. Researchers say time spent sitting was independently associated with total mortality, regardless of physical activity level. They conclude that public health messages should promote both being physically active and reducing time spent sitting. The study appears early online in the American Journal of Epidemiology.
Increasing obesity levels in the United States are widely predicted to have major public health consequences. A growing epidemic of overweight and obesity has been attributed in part to reduced overall physical activity. And while several studies support a link between sitting time and obesity, type 2 diabetes, cardiovascular disease risk factors (11, 16, 17), and unhealthy dietary patterns in children and adults (18-20), very few studies have examined time spent sitting in relation to total mortality (21-23). Thus, public health guidelines focus largely on increasing physical activity with little or no reference to reducing time spent sitting.
To explore the association between sitting time and mortality, researchers led by Alpa Patel, Ph.D. analyzed survey responses from 123,216 individuals (53,440 men and 69,776 women) who had no history of cancer, heart attack, stroke, or emphysema/other lung disease enrolled in the American Cancer Society's Cancer Prevention II study in 1992. They examined the amount of time spent sitting and physical activity in relation to mortality between 1993 and 2006. They found that more leisure time spent sitting was associated with higher risk of mortality, particularly in women. Women who reported more than six hours per day of sitting were 37 percent more likely to die during the time period studied than those who sat fewer than 3 hours a day. Men who sat more than 6 hours a day were 18 percent more likely to die than those who sat fewer than 3 hours per day. The association remained virtually unchanged after adjusting for physical activity level. Associations were stronger for cardiovascular disease mortality than for cancer mortality.
When combined with a lack of physical activity, the association was even stronger. Women and men who both sat more and were less physically were 94% and 48% more likely, respectively, to die compared with those who reported sitting the least and being most active.
"Several factors could explain the positive association between time spent sitting and higher all-cause death rates," said Dr. Patel. "Prolonged time spent sitting, independent of physical activity, has been shown to have important metabolic consequences, and may influence things like triglycerides, high density lipoprotein, cholesterol, fasting plasma glucose, resting blood pressure, and leptin, which are biomarkers of obesity and cardiovascular and other chronic diseases."
The authors conclude that "public health messages and guidelines should be refined to include reducing time spent sitting in addition to promoting physical activity. Because a sizeable fraction of the population spends much of their time sitting, it is beneficial to encourage sedentary individuals to stand up and walk around as well as to reach optimal levels of physical activity."
Does Cleaning Cause Breast Cancer?
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Women who report greater use of cleaning products may be at higher breast cancer risk than those who say they use them sparingly. Researchers writing in BioMed Central's open access journal Environmental Health asked more than 1500 women about their cleaning product usage and found that women who reported using more air fresheners and products for mold and mildew control had a higher incidence of breast cancer.
Julia Brody, from the Silent Spring Institute, USA, worked with a team of researchers to carry out telephone interviews with 787 women diagnosed with breast cancer and 721 comparison women. She said, "Women who reported the highest combined cleaning product use had a doubled risk of breast cancer compared to those with the lowest reported use. Use of air fresheners and products for mold and mildew control were associated with increased risk. To our knowledge, this is the first published report on cleaning product use and risk of breast cancer."
The researchers questioned women on product use, beliefs about breast cancer causes, and established and suspected risk factors. They found that cleaning products, air fresheners, and insect repellents were associated with breast cancer, but little association was observed with overall pesticide use. Women with breast cancer who believed that chemicals and pollutants contribute 'a lot' to the risk of developing the condition were more likely to report high product usage.
Speaking about this potential bias to the study, Brody said, "When women are diagnosed with breast cancer, they often think about what happened in the past that might have contributed to the disease. As a result, it may be that women with breast cancer more accurately recall their past product use or even over-estimate it. Or, it could also be that experience with breast cancer influences beliefs about its causes. For example, women diagnosed with breast cancer are less likely to believe heredity contributes 'a lot', because most are the first in their family to get the disease."
In order to avoid possible recall bias, the researchers recommend further study of cleaning products and breast cancer using prospective self-reports and measurements in environmental and biological media.
Women who report greater use of cleaning products may be at higher breast cancer risk than those who say they use them sparingly. Researchers writing in BioMed Central's open access journal Environmental Health asked more than 1500 women about their cleaning product usage and found that women who reported using more air fresheners and products for mold and mildew control had a higher incidence of breast cancer.
Julia Brody, from the Silent Spring Institute, USA, worked with a team of researchers to carry out telephone interviews with 787 women diagnosed with breast cancer and 721 comparison women. She said, "Women who reported the highest combined cleaning product use had a doubled risk of breast cancer compared to those with the lowest reported use. Use of air fresheners and products for mold and mildew control were associated with increased risk. To our knowledge, this is the first published report on cleaning product use and risk of breast cancer."
The researchers questioned women on product use, beliefs about breast cancer causes, and established and suspected risk factors. They found that cleaning products, air fresheners, and insect repellents were associated with breast cancer, but little association was observed with overall pesticide use. Women with breast cancer who believed that chemicals and pollutants contribute 'a lot' to the risk of developing the condition were more likely to report high product usage.
Speaking about this potential bias to the study, Brody said, "When women are diagnosed with breast cancer, they often think about what happened in the past that might have contributed to the disease. As a result, it may be that women with breast cancer more accurately recall their past product use or even over-estimate it. Or, it could also be that experience with breast cancer influences beliefs about its causes. For example, women diagnosed with breast cancer are less likely to believe heredity contributes 'a lot', because most are the first in their family to get the disease."
In order to avoid possible recall bias, the researchers recommend further study of cleaning products and breast cancer using prospective self-reports and measurements in environmental and biological media.
Wednesday, July 21, 2010
New evidence that chili pepper ingredient fights fat
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Capsaicin, the stuff that gives chili peppers their kick, may cause weight loss and fight fat buildup by triggering certain beneficial protein changes in the body, according to a new study on the topic. The report, which could lead to new treatments for obesity, appears in ACS' monthly Journal of Proteome Research.
Jong Won Yun and colleagues point out that obesity is a major public health threat worldwide, linked to diabetes, high blood pressure, heart disease, and other health problems. Laboratory studies have hinted that capsaicin may help fight obesity by decreasing calorie intake, shrinking fat tissue, and lowering fat levels in the blood. Nobody, however, knows exactly how capsaicin might trigger such beneficial effects.
In an effort to find out, the scientists fed high-fat diets with or without capsaicin to lab rats used to study obesity. The capsaicin-treated rats lost 8 percent of their body weight and showed changes in levels of at least 20 key proteins found in fat. The altered proteins work to break down fats. "These changes provide valuable new molecular insights into the mechanism of the antiobesity effects of capsaicin," the scientists say.
Capsaicin, the stuff that gives chili peppers their kick, may cause weight loss and fight fat buildup by triggering certain beneficial protein changes in the body, according to a new study on the topic. The report, which could lead to new treatments for obesity, appears in ACS' monthly Journal of Proteome Research.
Jong Won Yun and colleagues point out that obesity is a major public health threat worldwide, linked to diabetes, high blood pressure, heart disease, and other health problems. Laboratory studies have hinted that capsaicin may help fight obesity by decreasing calorie intake, shrinking fat tissue, and lowering fat levels in the blood. Nobody, however, knows exactly how capsaicin might trigger such beneficial effects.
In an effort to find out, the scientists fed high-fat diets with or without capsaicin to lab rats used to study obesity. The capsaicin-treated rats lost 8 percent of their body weight and showed changes in levels of at least 20 key proteins found in fat. The altered proteins work to break down fats. "These changes provide valuable new molecular insights into the mechanism of the antiobesity effects of capsaicin," the scientists say.
Monday, July 19, 2010
What does the research say to do to avoid dementia and Alzheimers?
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A reader of my Health News Reports has asked:
Other than physical exercise and moderate drinking, what else is there to do to avoid dementia and Alzheimers?
Here are the relevant research reports:
Eating foods rich in vitamin E associated with lower dementia risk
High blood levels of vitamin E reduces risk of Alzheimer's
Vitamin D Promotes Mental Agility in Elders
Abdominal fat at middle age associated with greater risk of dementia
Caffeine may slow Alzheimer's disease and other dementias, restore cognitive function
Magnesium Helps You Remember - But Not Supplements
High fruit/vegetable = high cognitive performance
Mediterranean Diet = Slower Cognitive Decline
Mediterranean diet, exercise fight Alzheimer disease
Methionine could increase risk of Alzheimer’s
Other possible help; Green tea, dark chocolate, grapes, apple juice (references upon request.)
A reader of my Health News Reports has asked:
Other than physical exercise and moderate drinking, what else is there to do to avoid dementia and Alzheimers?
Here are the relevant research reports:
Eating foods rich in vitamin E associated with lower dementia risk
High blood levels of vitamin E reduces risk of Alzheimer's
Vitamin D Promotes Mental Agility in Elders
Abdominal fat at middle age associated with greater risk of dementia
Caffeine may slow Alzheimer's disease and other dementias, restore cognitive function
Magnesium Helps You Remember - But Not Supplements
Dr. Slutsky advises people to get their magnesium the old-fashioned way — by eating lots of green leaves, broccoli, almonds, cashews and fruit. The effects on memory won't appear overnight, she cautions, but with this persistent change in diet, memory should improve, and the effects of dementia and other cognitive impairment diseases related to aging may be considerably delayed.
High fruit/vegetable = high cognitive performance
Results published in the August issue of the Journal of Alzheimer's Disease indicated higher cognitive performance in individuals with high daily intake of fruits and vegetables.
Mediterranean Diet = Slower Cognitive Decline
Higher adherence to a Mediterranean-type diet is linked to lower risk for mortality and chronic diseases. In an examination of the association between adherence to a Mediterranean-type diet and cognitive performance and risk of dementia, researchers found that high adherence to the diet was associated with slower decline in some measures of cognitive function.
Mediterranean diet, exercise fight Alzheimer disease
Elderly individuals who had a diet that included higher consumption of fruits, vegetables, legumes, cereal and fish and was low in red meat and poultry and who were physically active had an associated lower risk of Alzheimer disease.
Methionine could increase risk of Alzheimer’s
A diet rich in methionine, an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds, can possibly increase the risk of developing Alzheimer’s disease, according to a study by Temple researchers.
Still, Praticò emphasized, methionine is an essential amino acid for the human body and “stopping one’s intake of methionine won’t prevent Alzheimer’s. But people who have a diet high in red meat, for instance, could be more at risk because they are more likely to develop this high level of circulating homocysteine,” he said.
Other possible help; Green tea, dark chocolate, grapes, apple juice (references upon request.)
Thursday, July 15, 2010
Less salt for everybody
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Restricting the amount of sodium chloride in food can lower the risk of cardiovascular morbidities. This is the conclusion that Dieter Klaus and colleagues come to in the current issue of Deutsches Ärzteblatt International (Dtsch Arztebl Int 2010; 107[26]: 457-62).
People whose intake of dietary sodium chloride is in excess of 6 g per day increase their risk of cardiovascular morbidities and hypertension. This is particularly notable in view of the fact that in the Western industrialized nations, one in two deaths is due to a cardiovascular disorder and the average intake of sodium chloride is in the range of 8 to 12 g/d. Salt restriction may help not only to prevent cardiovascular morbidities but may also counteract other lifestyle diseases such as obesity and diabetes.
As a preventive measure, the authors suggest reducing dietary salt intake population-wide. By successively lowering the NaCl content of industrially processed foods by 40% to 50%, people's daily salt intake would be lowered to 5 to 6 g/d per head of population.
Restricting the amount of sodium chloride in food can lower the risk of cardiovascular morbidities. This is the conclusion that Dieter Klaus and colleagues come to in the current issue of Deutsches Ärzteblatt International (Dtsch Arztebl Int 2010; 107[26]: 457-62).
People whose intake of dietary sodium chloride is in excess of 6 g per day increase their risk of cardiovascular morbidities and hypertension. This is particularly notable in view of the fact that in the Western industrialized nations, one in two deaths is due to a cardiovascular disorder and the average intake of sodium chloride is in the range of 8 to 12 g/d. Salt restriction may help not only to prevent cardiovascular morbidities but may also counteract other lifestyle diseases such as obesity and diabetes.
As a preventive measure, the authors suggest reducing dietary salt intake population-wide. By successively lowering the NaCl content of industrially processed foods by 40% to 50%, people's daily salt intake would be lowered to 5 to 6 g/d per head of population.
Only 10 percent or less of older children, men, women and pregnant women in America are meeting the Adequate Intake (AI) levels for choline
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A study published in the American Journal of Clinical Nutrition found that a choline-deficient diet is associated with increased risk for heart defects during prenatal development. Choline is an essential nutrient required for normal cell activity, healthy brain and nerve function, liver metabolism and transportation of nutrients throughout the body. Research shows that only 10 percent or less of older children, men, women and pregnant women in America are meeting the Adequate Intake (AI) levels for choline; despite a growing body of science which supports the importance of choline especially in healthy fetal development.
The Importance of Choline Throughout the Lifespan
A study published in the American Journal of Clinical Nutrition examined adult dietary intake of choline and betaine (a nutrient related to choline) and found that higher intakes of choline and betaine were associated with lower blood homocysteine concentrations, especially in subjects with low blood levels of folate and vitamin B12.4 Choline, like folate, is involved in breaking down homocysteine in the blood. Elevated homocysteine concentrations have been associated with increased risk of stroke, coronary heart disease and cognitive decline.
In May, a study published online in the Journal of Nutrition reported on the role of choline in the complex system that regulates DNA production and stability. Researchers studied the impact of choline intake on DNA damage in 60 Mexican-American men. They found that individuals with greater intakes of choline, even exceeding current dietary recommendations, exhibited the least amount of DNA damage.
Vital Role of Choline During Pregnancy
A growing body of science, conducted in both animals and humans, supports the need for more dietary choline. Researchers from McGill University and Cornell University examined the offspring of mice that consumed a choline-deficient diet during pregnancy compared to the offspring of mice that consumed a diet containing the recommended amount of choline. The researchers observed that heart defects were more prevalent among the offspring of mice consuming a choline-deficient diet. The study also found that low choline intake was associated with increased levels of homocysteine, an amino acid in the blood that, when elevated, is associated with an increased risk of cardiovascular disease and declined cognitive function.
"Choline is a complex nutrient that is intricately involved in fetal development, and this research reveals another piece of the puzzle,"according to Cornell University Associate Professor, Marie Caudill, Ph.D., R.D. "Women with diets low in choline have two times greater risk of having babies with neural tube defects so it's essential that nutrition education during pregnancy and breastfeeding highlight the importance of dietary sources of choline."
Another study, published in the June issue of Behavioral Neuroscience, reported that choline intake during pregnancy and lactation is associated with improved attention function. The researchers observed that offspring of female mice consuming a diet supplemented with choline during pregnancy and lactation performed significantly better on attention tasks compared to offspring from mothers consuming a diet not supplemented with choline.
Focusing on a Choline-Rich Diet
"Choline is important for people of all ages, particularly moms and moms-to-be," says Neva Cochran, M.S., R.D., nutrition communications consultant and nutrition writer and researcher for Woman's World magazine. "It is easy to meet the recommended choline intake with delicious foods like an egg, which is an excellent source of choline and provides roughly one-quarter of a pregnant or breastfeeding woman's choline needs."
Eggs, soy, peanuts and almonds are good sources of choline.
Strict vegetarians who avoid all animal products, endurance athletes and people who drink a lot of alcohol may be at risk for choline deficiency and may benefit from choline supplements.
A study published in the American Journal of Clinical Nutrition found that a choline-deficient diet is associated with increased risk for heart defects during prenatal development. Choline is an essential nutrient required for normal cell activity, healthy brain and nerve function, liver metabolism and transportation of nutrients throughout the body. Research shows that only 10 percent or less of older children, men, women and pregnant women in America are meeting the Adequate Intake (AI) levels for choline; despite a growing body of science which supports the importance of choline especially in healthy fetal development.
The Importance of Choline Throughout the Lifespan
A study published in the American Journal of Clinical Nutrition examined adult dietary intake of choline and betaine (a nutrient related to choline) and found that higher intakes of choline and betaine were associated with lower blood homocysteine concentrations, especially in subjects with low blood levels of folate and vitamin B12.4 Choline, like folate, is involved in breaking down homocysteine in the blood. Elevated homocysteine concentrations have been associated with increased risk of stroke, coronary heart disease and cognitive decline.
In May, a study published online in the Journal of Nutrition reported on the role of choline in the complex system that regulates DNA production and stability. Researchers studied the impact of choline intake on DNA damage in 60 Mexican-American men. They found that individuals with greater intakes of choline, even exceeding current dietary recommendations, exhibited the least amount of DNA damage.
Vital Role of Choline During Pregnancy
A growing body of science, conducted in both animals and humans, supports the need for more dietary choline. Researchers from McGill University and Cornell University examined the offspring of mice that consumed a choline-deficient diet during pregnancy compared to the offspring of mice that consumed a diet containing the recommended amount of choline. The researchers observed that heart defects were more prevalent among the offspring of mice consuming a choline-deficient diet. The study also found that low choline intake was associated with increased levels of homocysteine, an amino acid in the blood that, when elevated, is associated with an increased risk of cardiovascular disease and declined cognitive function.
"Choline is a complex nutrient that is intricately involved in fetal development, and this research reveals another piece of the puzzle,"according to Cornell University Associate Professor, Marie Caudill, Ph.D., R.D. "Women with diets low in choline have two times greater risk of having babies with neural tube defects so it's essential that nutrition education during pregnancy and breastfeeding highlight the importance of dietary sources of choline."
Another study, published in the June issue of Behavioral Neuroscience, reported that choline intake during pregnancy and lactation is associated with improved attention function. The researchers observed that offspring of female mice consuming a diet supplemented with choline during pregnancy and lactation performed significantly better on attention tasks compared to offspring from mothers consuming a diet not supplemented with choline.
Focusing on a Choline-Rich Diet
"Choline is important for people of all ages, particularly moms and moms-to-be," says Neva Cochran, M.S., R.D., nutrition communications consultant and nutrition writer and researcher for Woman's World magazine. "It is easy to meet the recommended choline intake with delicious foods like an egg, which is an excellent source of choline and provides roughly one-quarter of a pregnant or breastfeeding woman's choline needs."
Eggs, soy, peanuts and almonds are good sources of choline.
Strict vegetarians who avoid all animal products, endurance athletes and people who drink a lot of alcohol may be at risk for choline deficiency and may benefit from choline supplements.
Cranberry Juice Fights Bacteria at the Molecular Level
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Revealing the science behind the homespun advice, a team of researchers at Worcester Polytechnic Institute (WPI) has identified and measured the molecular forces that enable cranberry juice to fight off urinary tract infections in people.
The data is reported in the paper "Direct adhesion force measurements between E. coli and human uroepithelial cells in cranberry juice cocktail," which was published on-line, ahead of print, by the journal Molecular Nutrition and Food Research. The research illuminates the basic mechanics of E. coli infections, which has implications for developing new antibiotic drugs and infection-resistant materials for invasive medical devices.
The research team led by Terri Camesano, professor of chemical engineering at WPI, focuses on the virulent form of E. coli bacteria that is the primary cause of most urinary tract infections. This strain of E. coli is covered with small hair-like projections known as fimbriae which act like hooks and latch onto cells that line the urinary tract. When enough of the virulent E. coli adhere to cells in this way, they cause an infection. Previous work by Camesano has shown that exposure to cranberry juice causes the fimbriae on E. coli to curl up, reducing their ability to attach to urinary tract cells. In the new study, Camesano's team presents the first specific measurements of the mechanical forces involved in the attachment of the virulent E. coli to human urinary tract cells. The study also documents how the force of attachment is reduced in the presence of cranberry juice cocktail. "This is not a clinical study—it's a mechanical study that shows us the direct forces that can lead to infection," Camesano said.
To make measurements at the molecular level, Camesano's team developed a method to attach a single E. coli cell to the tip of a probe mounted on a device called an atomic force microscope (AFM). The probe was then dipped in a solution containing human uroepithelial cells, which line the urinary tract. The fimbriae on the E. coli latched onto to specific structures on the human cells, similar to the way the two halves of a Velcro fastener come together. The probe on the AFM was then pulled away from the human cells, measuring the amount of force needed to tear the E. coli away. "We know, on average, how many fimbriae are on each E. coli cell. And the total force we measured correlates with that number. So the data lead us to believe that the fimbriae each bind to a specific receptor on the uroepithelial cells," Camesano said.
The experiment was repeated numerous times with solutions containing human cells and various concentrations of commercially available cranberry juice cocktail. The data showed that the attachment force of the virulent E. coli weakened as the amount of cranberry juice cocktail increased. The study also showed that a strain of E. coli without fimbriae did not bind well to the human urinary tract cells, regardless of the concentration of cranberry juice cocktail, providing further evidence that fimbriae are essential for infection.
Furthermore, Camesano's team found that in the absence of cranberry juice, the strength of the virulent E. coli's bond to the human cells was so strong that it could not be broken by the typical force of urine flowing through a person's urinary tract. However, as the cranberry juice concentration increased, the bond weakened to the point where the E.coli could be stripped away by the force of flowing urine. "The shear force created by flowing urine is a defense mechanism against urinary tract infection," Camesano said.
Since bacterial adhesion is required for infection, Camesano said understanding the specific mechanisms and forces involved will help direct future studies aimed at identifying potential drug targets for new antibiotics. The data may also be useful in studies aimed at engineering the surfaces of invasive medical devices like catheters to make them more resistant to bacterial adhesion.
Revealing the science behind the homespun advice, a team of researchers at Worcester Polytechnic Institute (WPI) has identified and measured the molecular forces that enable cranberry juice to fight off urinary tract infections in people.
The data is reported in the paper "Direct adhesion force measurements between E. coli and human uroepithelial cells in cranberry juice cocktail," which was published on-line, ahead of print, by the journal Molecular Nutrition and Food Research. The research illuminates the basic mechanics of E. coli infections, which has implications for developing new antibiotic drugs and infection-resistant materials for invasive medical devices.
The research team led by Terri Camesano, professor of chemical engineering at WPI, focuses on the virulent form of E. coli bacteria that is the primary cause of most urinary tract infections. This strain of E. coli is covered with small hair-like projections known as fimbriae which act like hooks and latch onto cells that line the urinary tract. When enough of the virulent E. coli adhere to cells in this way, they cause an infection. Previous work by Camesano has shown that exposure to cranberry juice causes the fimbriae on E. coli to curl up, reducing their ability to attach to urinary tract cells. In the new study, Camesano's team presents the first specific measurements of the mechanical forces involved in the attachment of the virulent E. coli to human urinary tract cells. The study also documents how the force of attachment is reduced in the presence of cranberry juice cocktail. "This is not a clinical study—it's a mechanical study that shows us the direct forces that can lead to infection," Camesano said.
To make measurements at the molecular level, Camesano's team developed a method to attach a single E. coli cell to the tip of a probe mounted on a device called an atomic force microscope (AFM). The probe was then dipped in a solution containing human uroepithelial cells, which line the urinary tract. The fimbriae on the E. coli latched onto to specific structures on the human cells, similar to the way the two halves of a Velcro fastener come together. The probe on the AFM was then pulled away from the human cells, measuring the amount of force needed to tear the E. coli away. "We know, on average, how many fimbriae are on each E. coli cell. And the total force we measured correlates with that number. So the data lead us to believe that the fimbriae each bind to a specific receptor on the uroepithelial cells," Camesano said.
The experiment was repeated numerous times with solutions containing human cells and various concentrations of commercially available cranberry juice cocktail. The data showed that the attachment force of the virulent E. coli weakened as the amount of cranberry juice cocktail increased. The study also showed that a strain of E. coli without fimbriae did not bind well to the human urinary tract cells, regardless of the concentration of cranberry juice cocktail, providing further evidence that fimbriae are essential for infection.
Furthermore, Camesano's team found that in the absence of cranberry juice, the strength of the virulent E. coli's bond to the human cells was so strong that it could not be broken by the typical force of urine flowing through a person's urinary tract. However, as the cranberry juice concentration increased, the bond weakened to the point where the E.coli could be stripped away by the force of flowing urine. "The shear force created by flowing urine is a defense mechanism against urinary tract infection," Camesano said.
Since bacterial adhesion is required for infection, Camesano said understanding the specific mechanisms and forces involved will help direct future studies aimed at identifying potential drug targets for new antibiotics. The data may also be useful in studies aimed at engineering the surfaces of invasive medical devices like catheters to make them more resistant to bacterial adhesion.
Wednesday, July 14, 2010
Low vitamin D levels associated with cognitive decline
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Older adults with low levels of vitamin D appear more likely to experience declines in thinking, learning and memory over a six-year period, according to a report in the July 12 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
An estimated 40 percent to 100 percent of older adults in the United States and Europe are deficient in vitamin D, according to background information in the article. This deficiency has been linked to fractures, various chronic diseases and death. Vitamin D may help prevent the degeneration of brain tissue by having a role in formation of nervous tissue, maintaining levels of calcium in the body, or clearing of beta-amyloid, the substance that forms the brain plaques and tangles associated with Alzheimer's disease.
David J. Llewellyn, Ph.D., of University of Exeter, England, and colleagues assessed blood levels of vitamin D in 858 adults who were age 65 or older when the study began in 1998. Participants completed interviews and medical examinations and provided blood samples. At the beginning of the study and again after three and six years, they repeated three tests of cognitive function—one assessing overall cognition, one focusing on attention and one that places greater emphasis on executive function, or the ability to plan, organize and prioritize.
Participants who were severely deficient in vitamin D (having blood levels of 25-hydroxyvitamin D of less than 25 nanomoles per liter) were 60 percent more likely to have substantial cognitive decline in general over the six-year period and 31 percent more likely to experience declines on the test measuring executive function than those with sufficient vitamin D levels. "The association remained significant after adjustment for a wide range of potential confounders and when analyses were restricted to elderly subjects who were non-demented at baseline," the authors write. However, no significant association was seen for the test measuring attention.
"If future prospective studies and randomized controlled trials confirm that vitamin D deficiency is causally related to cognitive decline, then this would open up important new possibilities for treatment and prevention," the authors conclude.
(Arch Intern Med. 2010;170[13]:1135-1141. Available pre-embargo to the media at www.jamamedia.org.)
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Editorial: Randomized Controlled Trials Needed to Examine Vitamin D's Role
"Vitamin D has been known for many years to play a critical role in skeletal health, such that very low levels of this hormone (less than 20 nanomoles per liter) can cause osteomalacia, a disorder of impaired bone mineralization," write Andrew Grey, M.D., and Mark Bolland, M.B.Ch.B., Ph.D., of University of Auckland, New Zealand, in an accompanying editorial. "More recently, observational studies have reported inverse associations between levels of serum 25-hydroxyvitamin D, the metabolite that best reflects overall vitamin D status, and the risk of a wide range of disease, including cancer, vascular disease, infectious conditions, autoimmune diseases, osteoporosis, type 2 diabetes mellitus and obesity."
"The results of these observational studies have prompted calls for widespread treatment of individuals with low levels of vitamin D and the establishment of public health programs aimed at raising the population levels of vitamin D to 'healthy' values," the authors write.
"It is now time to test the various hypotheses generated by observational studies of vitamin D, including that of Llewellyn et al, in adequately designed and conducted randomized controlled trials," they conclude. "Very importantly, such trials will also provide an opportunity to systematically assess potential harms of vitamin D supplementation, an issue that has been largely overlooked or dismissed. We should invest in trials that provide the best possible evidence on the benefits and risks of vitamin D before we invest in costly, difficult and potentially unrewarding interventional strategies."
Older adults with low levels of vitamin D appear more likely to experience declines in thinking, learning and memory over a six-year period, according to a report in the July 12 issue of Archives of Internal Medicine, one of the JAMA/Archives journals.
An estimated 40 percent to 100 percent of older adults in the United States and Europe are deficient in vitamin D, according to background information in the article. This deficiency has been linked to fractures, various chronic diseases and death. Vitamin D may help prevent the degeneration of brain tissue by having a role in formation of nervous tissue, maintaining levels of calcium in the body, or clearing of beta-amyloid, the substance that forms the brain plaques and tangles associated with Alzheimer's disease.
David J. Llewellyn, Ph.D., of University of Exeter, England, and colleagues assessed blood levels of vitamin D in 858 adults who were age 65 or older when the study began in 1998. Participants completed interviews and medical examinations and provided blood samples. At the beginning of the study and again after three and six years, they repeated three tests of cognitive function—one assessing overall cognition, one focusing on attention and one that places greater emphasis on executive function, or the ability to plan, organize and prioritize.
Participants who were severely deficient in vitamin D (having blood levels of 25-hydroxyvitamin D of less than 25 nanomoles per liter) were 60 percent more likely to have substantial cognitive decline in general over the six-year period and 31 percent more likely to experience declines on the test measuring executive function than those with sufficient vitamin D levels. "The association remained significant after adjustment for a wide range of potential confounders and when analyses were restricted to elderly subjects who were non-demented at baseline," the authors write. However, no significant association was seen for the test measuring attention.
"If future prospective studies and randomized controlled trials confirm that vitamin D deficiency is causally related to cognitive decline, then this would open up important new possibilities for treatment and prevention," the authors conclude.
(Arch Intern Med. 2010;170[13]:1135-1141. Available pre-embargo to the media at www.jamamedia.org.)
Editor's Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc.
Editorial: Randomized Controlled Trials Needed to Examine Vitamin D's Role
"Vitamin D has been known for many years to play a critical role in skeletal health, such that very low levels of this hormone (less than 20 nanomoles per liter) can cause osteomalacia, a disorder of impaired bone mineralization," write Andrew Grey, M.D., and Mark Bolland, M.B.Ch.B., Ph.D., of University of Auckland, New Zealand, in an accompanying editorial. "More recently, observational studies have reported inverse associations between levels of serum 25-hydroxyvitamin D, the metabolite that best reflects overall vitamin D status, and the risk of a wide range of disease, including cancer, vascular disease, infectious conditions, autoimmune diseases, osteoporosis, type 2 diabetes mellitus and obesity."
"The results of these observational studies have prompted calls for widespread treatment of individuals with low levels of vitamin D and the establishment of public health programs aimed at raising the population levels of vitamin D to 'healthy' values," the authors write.
"It is now time to test the various hypotheses generated by observational studies of vitamin D, including that of Llewellyn et al, in adequately designed and conducted randomized controlled trials," they conclude. "Very importantly, such trials will also provide an opportunity to systematically assess potential harms of vitamin D supplementation, an issue that has been largely overlooked or dismissed. We should invest in trials that provide the best possible evidence on the benefits and risks of vitamin D before we invest in costly, difficult and potentially unrewarding interventional strategies."
Eating foods rich in vitamin E associated with lower dementia risk
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Consuming more vitamin E through the diet appears to be associated with a lower risk of dementia and Alzheimer's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.
Oxidative stress—damage to the cells from oxygen exposure—is thought to play a role in the development of Alzheimer's disease, according to background information in the article. Experimental data suggest that antioxidants, nutrients that help repair this damage, may protect against the degeneration of nervous system cells. "Although clinical trials have shown no benefit of antioxidant supplements for Alzheimer's disease, the wider variety of antioxidants in food sources is not well studied relative to dementia risk; a few studies, with varying lengths of follow-up, have yielded inconsistent results," the authors write.
Elizabeth E. Devore, Sc.D., of Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues assessed 5,395 participants 55 years and older who did not have dementia between 1990 and 1993. Participants underwent a home interview and two clinical examinations at the beginning of the study, and provided dietary information through a two-step process involving a meal-based checklist and a food questionnaire.
The researchers focused on four antioxidants: vitamin E, vitamin C, beta carotene and flavonoids. The major food sources of vitamin E were margarine, sunflower oil, butter, cooking fat, soybean oil and mayonnaise; vitamin C came mainly from oranges, kiwi, grapefruit juice, grapefruit, cauliflower, red bell peppers and red cabbage; beta carotene, from carrots, spinach, vegetable soup, endive and tomato; and flavonoids from tea, onions, apples and carrots.
Over an average of 9.6 years of follow-up, 465 participants developed dementia; 365 of those were diagnosed with Alzheimer's disease. After adjusting for other potentially related factors, the one-third of individuals who consumed the most vitamin E (a median or midpoint of 18.5 milligrams per day) were 25 percent less likely to develop dementia than the one-third of participants who consumed the least (a median of 9 milligrams per day). Dietary intake levels of vitamin C, beta carotene and flavonoids were not associated with dementia risk. Results were similar when only the participants diagnosed with Alzheimer's disease were assessed.
"The brain is a site of high metabolic activity, which makes it vulnerable to oxidative damage, and slow accumulation of such damage over a lifetime may contribute to the development of dementia," the authors write. "In particular, when beta-amyloid (a hallmark of pathologic Alzheimer's disease) accumulates in the brain, an inflammatory response is likely evoked that produces nitric oxide radicals and downstream neurodegenerative effects. Vitamin E is a powerful fat-soluble antioxidant that may help to inhibit the pathogenesis of dementia."
Future studies are needed to evaluate dietary intake of antioxidants and dietary risks, including different points at which consuming more antioxidants might reduce risk, the authors conclude.
Consuming more vitamin E through the diet appears to be associated with a lower risk of dementia and Alzheimer's disease, according to a report in the July issue of Archives of Neurology, one of the JAMA/Archives journals.
Oxidative stress—damage to the cells from oxygen exposure—is thought to play a role in the development of Alzheimer's disease, according to background information in the article. Experimental data suggest that antioxidants, nutrients that help repair this damage, may protect against the degeneration of nervous system cells. "Although clinical trials have shown no benefit of antioxidant supplements for Alzheimer's disease, the wider variety of antioxidants in food sources is not well studied relative to dementia risk; a few studies, with varying lengths of follow-up, have yielded inconsistent results," the authors write.
Elizabeth E. Devore, Sc.D., of Erasmus Medical Center, Rotterdam, the Netherlands, and colleagues assessed 5,395 participants 55 years and older who did not have dementia between 1990 and 1993. Participants underwent a home interview and two clinical examinations at the beginning of the study, and provided dietary information through a two-step process involving a meal-based checklist and a food questionnaire.
The researchers focused on four antioxidants: vitamin E, vitamin C, beta carotene and flavonoids. The major food sources of vitamin E were margarine, sunflower oil, butter, cooking fat, soybean oil and mayonnaise; vitamin C came mainly from oranges, kiwi, grapefruit juice, grapefruit, cauliflower, red bell peppers and red cabbage; beta carotene, from carrots, spinach, vegetable soup, endive and tomato; and flavonoids from tea, onions, apples and carrots.
Over an average of 9.6 years of follow-up, 465 participants developed dementia; 365 of those were diagnosed with Alzheimer's disease. After adjusting for other potentially related factors, the one-third of individuals who consumed the most vitamin E (a median or midpoint of 18.5 milligrams per day) were 25 percent less likely to develop dementia than the one-third of participants who consumed the least (a median of 9 milligrams per day). Dietary intake levels of vitamin C, beta carotene and flavonoids were not associated with dementia risk. Results were similar when only the participants diagnosed with Alzheimer's disease were assessed.
"The brain is a site of high metabolic activity, which makes it vulnerable to oxidative damage, and slow accumulation of such damage over a lifetime may contribute to the development of dementia," the authors write. "In particular, when beta-amyloid (a hallmark of pathologic Alzheimer's disease) accumulates in the brain, an inflammatory response is likely evoked that produces nitric oxide radicals and downstream neurodegenerative effects. Vitamin E is a powerful fat-soluble antioxidant that may help to inhibit the pathogenesis of dementia."
Future studies are needed to evaluate dietary intake of antioxidants and dietary risks, including different points at which consuming more antioxidants might reduce risk, the authors conclude.
No evidence that popular slimming supplements facilitate weight loss
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New research evaluating the effectiveness of a broad selection of popular slimming supplements sold in pharmacies and health food shops has found no evidence that any of them facilitate weight loss beyond the placebo effect.
Two studies presented today (Monday) at the International Congress on Obesity in Stockholm, Sweden, have found they were no more effective than the fake supplements they were compared with.
"There are scores of slimming supplements out there claiming weight-loss effects through all sorts of mechanisms of action. We have so-called fat magnets, mobilizers and dissolvers, as well as appetite tamers, metabolism boosters, carb blockers and so on. The market for these is huge, but unlike for regulated drugs, effectiveness does not have to be proven for these to be sold," said Dr. Thomas Ellrott, head of the Institute for Nutrition and Psychology at the University of Göttingen Medical School, Germany, who lead one of the studies. "Few of these supplements have been submitted to clinical trials and the landscape of products is always changing, so we need to put them through rigorous scientific evaluation to determine whether they have any benefit."
Ellrott's group tested nine popular supplements against placebo pills in a randomized controlled trial. The supplements tested included L-Carnitine, polyglucosamine, cabbage powder, guarana seed powder, bean extract, Konjac extract, fibre pills, sodium alginate formulations and selected plant extracts.
The researchers bought the supplements from German pharmacies, changed the packaging and product names to make them look neutral and rewrote the information leaflet inserts to eliminate the product name from the text. They then gave 189 obese or overweight middle-aged consumers packages of either fake pills or of one of the nine supplements, each week for eight weeks, in doses recommended by the manufacturers. Some of the products came with dietary advice, while others didn't, so the researchers provided exactly the same advice as that written in the relevant product leaflets.
Average weight loss was between 1 kg and 2 kg across seven of the products, depending on the supplement, and was 1.2 kg in the group getting the placebo pills. No statistically significant difference in weight loss was found for any of those products when compared with the placebo.
"Most previous studies have examined only one product. This is the first to include nine supplements with different proposed mechanisms of action and we found that not a single product was any more effective than placebo pills in producing weight loss over the two months of the study, regardless of how it claims to work," Ellrott said, adding that if there is an indication for the use of weight-loss drugs, consumers should opt for regulated obesity drugs with proven effects (prescription or over-the-counter) instead.
In a second study presented at the congress, Dr. Igho Onakpoya of Peninsula Medical School at the Universities of Exeter and Plymouth, UK, conducted the first systematic review of all existing systematic reviews of clinical trials on weight loss supplements. The analysis summarizes the state of evidence from reviews of studies involving nine popular slimming supplements, including chromium picolinate, Ephedra, bitter orange, conjugated linoleic acid (CLA), calcium, guar gum, glucomannan, chitosan and green tea.
"We found no evidence that any of these food supplements studied is an adequate treatment for reducing body weight," Onakpoya said. "Annual global sales of dietary supplements are well over $13 billion. In Western Europe, sales of weight-loss products, excluding prescription medications, topped £900 million ($1.4 billion) in 2009. The weight-loss industry in North America is worth over $50 billion and Americans spend over $1.6 billion a year on weight-loss supplements. People think these supplements are a short cut to weight loss and may spend huge sums of money on them, but they may end up disappointed, frustrated and depressed if their weight expectations are not met in the long term."
Onakpoya said some of the supplements included the study were reported to cause some adverse effects. However, more rigorous research is needed, he said, as only very few trials have been of long duration and the number of patients in most of the trials has been small - factors which together limit the conclusions that can be drawn about the effectiveness and safety of such supplements.
Ellrott's study was funded by a German consumer issues magazine, while the study by Onakpoya and colleagues had no particular funding, but Onakpoya's position is funded by an unrestricted grant from GlaxoSmithkline, which makes the obesity drug orlistat.
New research evaluating the effectiveness of a broad selection of popular slimming supplements sold in pharmacies and health food shops has found no evidence that any of them facilitate weight loss beyond the placebo effect.
Two studies presented today (Monday) at the International Congress on Obesity in Stockholm, Sweden, have found they were no more effective than the fake supplements they were compared with.
"There are scores of slimming supplements out there claiming weight-loss effects through all sorts of mechanisms of action. We have so-called fat magnets, mobilizers and dissolvers, as well as appetite tamers, metabolism boosters, carb blockers and so on. The market for these is huge, but unlike for regulated drugs, effectiveness does not have to be proven for these to be sold," said Dr. Thomas Ellrott, head of the Institute for Nutrition and Psychology at the University of Göttingen Medical School, Germany, who lead one of the studies. "Few of these supplements have been submitted to clinical trials and the landscape of products is always changing, so we need to put them through rigorous scientific evaluation to determine whether they have any benefit."
Ellrott's group tested nine popular supplements against placebo pills in a randomized controlled trial. The supplements tested included L-Carnitine, polyglucosamine, cabbage powder, guarana seed powder, bean extract, Konjac extract, fibre pills, sodium alginate formulations and selected plant extracts.
The researchers bought the supplements from German pharmacies, changed the packaging and product names to make them look neutral and rewrote the information leaflet inserts to eliminate the product name from the text. They then gave 189 obese or overweight middle-aged consumers packages of either fake pills or of one of the nine supplements, each week for eight weeks, in doses recommended by the manufacturers. Some of the products came with dietary advice, while others didn't, so the researchers provided exactly the same advice as that written in the relevant product leaflets.
Average weight loss was between 1 kg and 2 kg across seven of the products, depending on the supplement, and was 1.2 kg in the group getting the placebo pills. No statistically significant difference in weight loss was found for any of those products when compared with the placebo.
"Most previous studies have examined only one product. This is the first to include nine supplements with different proposed mechanisms of action and we found that not a single product was any more effective than placebo pills in producing weight loss over the two months of the study, regardless of how it claims to work," Ellrott said, adding that if there is an indication for the use of weight-loss drugs, consumers should opt for regulated obesity drugs with proven effects (prescription or over-the-counter) instead.
In a second study presented at the congress, Dr. Igho Onakpoya of Peninsula Medical School at the Universities of Exeter and Plymouth, UK, conducted the first systematic review of all existing systematic reviews of clinical trials on weight loss supplements. The analysis summarizes the state of evidence from reviews of studies involving nine popular slimming supplements, including chromium picolinate, Ephedra, bitter orange, conjugated linoleic acid (CLA), calcium, guar gum, glucomannan, chitosan and green tea.
"We found no evidence that any of these food supplements studied is an adequate treatment for reducing body weight," Onakpoya said. "Annual global sales of dietary supplements are well over $13 billion. In Western Europe, sales of weight-loss products, excluding prescription medications, topped £900 million ($1.4 billion) in 2009. The weight-loss industry in North America is worth over $50 billion and Americans spend over $1.6 billion a year on weight-loss supplements. People think these supplements are a short cut to weight loss and may spend huge sums of money on them, but they may end up disappointed, frustrated and depressed if their weight expectations are not met in the long term."
Onakpoya said some of the supplements included the study were reported to cause some adverse effects. However, more rigorous research is needed, he said, as only very few trials have been of long duration and the number of patients in most of the trials has been small - factors which together limit the conclusions that can be drawn about the effectiveness and safety of such supplements.
Ellrott's study was funded by a German consumer issues magazine, while the study by Onakpoya and colleagues had no particular funding, but Onakpoya's position is funded by an unrestricted grant from GlaxoSmithkline, which makes the obesity drug orlistat.
Anti-cancer effects of broccoli ingredient explained
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Light has been cast on the interaction between broccoli consumption and reduced prostate cancer risk. Researchers writing in BioMed Central's open access journal Molecular Cancer have found that sulforaphane, a chemical found in broccoli, interacts with cells lacking a gene called PTEN to reduce the chances of prostate cancer developing.
Richard Mithen, from the Institute of Food Research, an institute of BBSRC, worked with a team of researchers on Norwich Research Park, UK, to carry out a series of experiments in human prostate tissue and mouse models of prostate cancer to investigate the interactions between expression of the PTEN gene and the anti-cancer activity of sulforaphane. He said, "PTEN is a tumour suppressor gene, the deletion or inactivation of which can initiate prostate carcinogenesis, and enhance the probability of cancer progression. We've shown here that sulforaphane has different effects depending on whether the PTEN gene is present".
The research team found that in cells which express PTEN, dietary intervention with SF has no effect on the development of cancer. In cells that don't express the gene, however, sulforaphane causes them to become less competitive, providing an explanation of how consuming broccoli can reduce the risk of prostate cancer incidence and progression. According to Mithen, "This also suggests potential therapeutic applications of sulforaphane and related compounds".
Light has been cast on the interaction between broccoli consumption and reduced prostate cancer risk. Researchers writing in BioMed Central's open access journal Molecular Cancer have found that sulforaphane, a chemical found in broccoli, interacts with cells lacking a gene called PTEN to reduce the chances of prostate cancer developing.
Richard Mithen, from the Institute of Food Research, an institute of BBSRC, worked with a team of researchers on Norwich Research Park, UK, to carry out a series of experiments in human prostate tissue and mouse models of prostate cancer to investigate the interactions between expression of the PTEN gene and the anti-cancer activity of sulforaphane. He said, "PTEN is a tumour suppressor gene, the deletion or inactivation of which can initiate prostate carcinogenesis, and enhance the probability of cancer progression. We've shown here that sulforaphane has different effects depending on whether the PTEN gene is present".
The research team found that in cells which express PTEN, dietary intervention with SF has no effect on the development of cancer. In cells that don't express the gene, however, sulforaphane causes them to become less competitive, providing an explanation of how consuming broccoli can reduce the risk of prostate cancer incidence and progression. According to Mithen, "This also suggests potential therapeutic applications of sulforaphane and related compounds".
New evidence shows low vitamin D levels lead to Parkinson's disease
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A new study on vitamin D levels and Parkinson's disease risk points to the need for further research on whether vitamin D supplements can protect against the movement disorder, according to an editorial in the July 2010 issue of Archives of Neurology.
The author of the editorial is Marian Evatt, MD, assistant professor of neurology at Emory University School of Medicine and director of the Atlanta Veterans Affairs Medical Center's Movement Disorders Clinic.
The study, also reported in Archives of Neurology, is the first to show that low vitamin D levels can help predict whether someone will later develop Parkinson's disease. Researchers at Finland's National Institute for Health and Welfare measured vitamin D levels from more than 3000 people, using blood samples taken between 1978 and 1980, and then followed those people to see whether they developed Parkinson's. People with the lowest levels of vitamin D were three times more likely to develop Parkinson's, compared to the group with the highest levels.
Previous research had suggested a link between low vitamin D and Parkinson's, but whether this is a cause-and-effect relationship is unknown. Vitamin D may help protect the population of neurons gradually lost by people with Parkinson's disease, Evatt writes in her editorial.
Parkinson's disease affects nerve cells in several parts of the brain, particularly those that use the chemical messenger dopamine to control movement. The most common symptoms are tremor, stiffness and slowness of movement. These can be treated with oral replacement of dopamine.
Research on animals suggests that vitamin D may protect neurons that produce dopamine from toxins. Besides vitamin D levels, factors such as genetics and exposure to pesticides also are associated with the risk for developing Parkinson's disease.
Doctors have known for decades that vitamin D promotes calcium uptake and bone formation, but evidence is accumulating for additional roles regulating the immune system and the development of the nervous system. Humans can get vitamin D from exposure to sunlight or eating foods such as fatty fish or fortified foods such as milk and packaged cereals. People living at high latitudes tend to have less exposure to the sun; in the Finnish study, the average vitamin D level was about half of the currently recommended level.
Vitamin D levels are usually measured by looking at the stable, 25-hydroxy form; the current recommended level is 30-40 nanograms per milliliter of blood.
Evatt writes that public health authorities should consider raising the target vitamin D level above the current recommended target because of known benefits for bone health as well as potential benefits for the nervous system. Still, animal data suggests that too much vitamin D can also be harmful for the nervous system, and megadoses of vitamin D can induce hypercalcemia, or an excess of calcium in the blood.
"At this point, 30 ng/ml or more appears optimal for bone health in humans. However, researchers don't yet know what level is optimal for brain health or at what point vitamin D becomes toxic for humans, and this is a topic that deserves close examination," she says.
A new study on vitamin D levels and Parkinson's disease risk points to the need for further research on whether vitamin D supplements can protect against the movement disorder, according to an editorial in the July 2010 issue of Archives of Neurology.
The author of the editorial is Marian Evatt, MD, assistant professor of neurology at Emory University School of Medicine and director of the Atlanta Veterans Affairs Medical Center's Movement Disorders Clinic.
The study, also reported in Archives of Neurology, is the first to show that low vitamin D levels can help predict whether someone will later develop Parkinson's disease. Researchers at Finland's National Institute for Health and Welfare measured vitamin D levels from more than 3000 people, using blood samples taken between 1978 and 1980, and then followed those people to see whether they developed Parkinson's. People with the lowest levels of vitamin D were three times more likely to develop Parkinson's, compared to the group with the highest levels.
Previous research had suggested a link between low vitamin D and Parkinson's, but whether this is a cause-and-effect relationship is unknown. Vitamin D may help protect the population of neurons gradually lost by people with Parkinson's disease, Evatt writes in her editorial.
Parkinson's disease affects nerve cells in several parts of the brain, particularly those that use the chemical messenger dopamine to control movement. The most common symptoms are tremor, stiffness and slowness of movement. These can be treated with oral replacement of dopamine.
Research on animals suggests that vitamin D may protect neurons that produce dopamine from toxins. Besides vitamin D levels, factors such as genetics and exposure to pesticides also are associated with the risk for developing Parkinson's disease.
Doctors have known for decades that vitamin D promotes calcium uptake and bone formation, but evidence is accumulating for additional roles regulating the immune system and the development of the nervous system. Humans can get vitamin D from exposure to sunlight or eating foods such as fatty fish or fortified foods such as milk and packaged cereals. People living at high latitudes tend to have less exposure to the sun; in the Finnish study, the average vitamin D level was about half of the currently recommended level.
Vitamin D levels are usually measured by looking at the stable, 25-hydroxy form; the current recommended level is 30-40 nanograms per milliliter of blood.
Evatt writes that public health authorities should consider raising the target vitamin D level above the current recommended target because of known benefits for bone health as well as potential benefits for the nervous system. Still, animal data suggests that too much vitamin D can also be harmful for the nervous system, and megadoses of vitamin D can induce hypercalcemia, or an excess of calcium in the blood.
"At this point, 30 ng/ml or more appears optimal for bone health in humans. However, researchers don't yet know what level is optimal for brain health or at what point vitamin D becomes toxic for humans, and this is a topic that deserves close examination," she says.
Tea contains more fluoride than once thought
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Black tea, a Southern staple and the world's most consumed beverage, may contain higher concentrations of fluoride than previously thought, which could pose problems for the heaviest tea drinkers, Medical College of Georgia researchers say.
"The additional fluoride from drinking two to four cups of tea a day won't harm anyone; it's the very heavy tea drinkers who could get in trouble," said Dr. Gary Whitford, Regents Professor of oral biology in the School of Dentistry. He presented his findings today at the 2010 International Association of Dental Research Conference in Barcelona, Spain.
Most published reports show 1 to 5 milligrams of fluoride per liter of black tea, but a new study shows that number could be as high as 9 milligrams.
Fluoride is known to help prevent dental cavities, but long-term ingestion of excessive amounts could cause bone problems. The average person ingests a very safe amount, 2 to 3 milligrams, daily through fluoridated drinking water, toothpaste and food. It would take ingesting about 20 milligrams a day over 10 or more years before posing a significant risk to bone health.
Whitford discovered that the fluoride concentration in black tea had long been underestimated when he began analyzing data from four patients with advanced skeletal fluorosis, a disease caused by excessive fluoride consumption and characterized by joint and bone pain and damage. While it is extremely rare in the United States, the common link between these four patients was their tea consumption – each person drank 1 to 2 gallons of tea daily for the past 10 to 30 years.
"When we tested the patients' tea brands using a traditional method, we found the fluoride concentrations to be very low, so we wondered if that method was detecting all of the fluoride," Whitford said, noting that the tea plant, Camellia sinensis, creates a quandary when measuring fluoride. Unique among other plants, it accumulates huge concentrations of fluoride and aluminum in its leaves – each mineral ranges from 600 to more than 1,000 milligrams per kilogram of leaves. When the leaves are brewed for tea, some of the minerals leach into the beverage.
Most published studies about black tea traditionally have used a method of measuring fluoride that doesn't account for the amount that combines with aluminum to form insoluble aluminum fluoride, which is not detected by the fluoride electrode. Whitford compared that method with a diffusion method, which breaks the aluminum-fluoride bond so that all fluoride in the tea samples can be extracted and measured.
He tested seven brands of store-bought black tea, steeping each for five minutes in deionized water, which contains no fluoride. The amount of fluoride in each sample was 1.4 to 3.3 times higher using the diffusion method than the traditional method.
The new information shouldn't deter tea drinkers, as the beverage is safe and some teas even have health benefits, Whitford said. "The bottom line is to enjoy your favorite tea, but like everything else, drink it in moderation."
Black tea, a Southern staple and the world's most consumed beverage, may contain higher concentrations of fluoride than previously thought, which could pose problems for the heaviest tea drinkers, Medical College of Georgia researchers say.
"The additional fluoride from drinking two to four cups of tea a day won't harm anyone; it's the very heavy tea drinkers who could get in trouble," said Dr. Gary Whitford, Regents Professor of oral biology in the School of Dentistry. He presented his findings today at the 2010 International Association of Dental Research Conference in Barcelona, Spain.
Most published reports show 1 to 5 milligrams of fluoride per liter of black tea, but a new study shows that number could be as high as 9 milligrams.
Fluoride is known to help prevent dental cavities, but long-term ingestion of excessive amounts could cause bone problems. The average person ingests a very safe amount, 2 to 3 milligrams, daily through fluoridated drinking water, toothpaste and food. It would take ingesting about 20 milligrams a day over 10 or more years before posing a significant risk to bone health.
Whitford discovered that the fluoride concentration in black tea had long been underestimated when he began analyzing data from four patients with advanced skeletal fluorosis, a disease caused by excessive fluoride consumption and characterized by joint and bone pain and damage. While it is extremely rare in the United States, the common link between these four patients was their tea consumption – each person drank 1 to 2 gallons of tea daily for the past 10 to 30 years.
"When we tested the patients' tea brands using a traditional method, we found the fluoride concentrations to be very low, so we wondered if that method was detecting all of the fluoride," Whitford said, noting that the tea plant, Camellia sinensis, creates a quandary when measuring fluoride. Unique among other plants, it accumulates huge concentrations of fluoride and aluminum in its leaves – each mineral ranges from 600 to more than 1,000 milligrams per kilogram of leaves. When the leaves are brewed for tea, some of the minerals leach into the beverage.
Most published studies about black tea traditionally have used a method of measuring fluoride that doesn't account for the amount that combines with aluminum to form insoluble aluminum fluoride, which is not detected by the fluoride electrode. Whitford compared that method with a diffusion method, which breaks the aluminum-fluoride bond so that all fluoride in the tea samples can be extracted and measured.
He tested seven brands of store-bought black tea, steeping each for five minutes in deionized water, which contains no fluoride. The amount of fluoride in each sample was 1.4 to 3.3 times higher using the diffusion method than the traditional method.
The new information shouldn't deter tea drinkers, as the beverage is safe and some teas even have health benefits, Whitford said. "The bottom line is to enjoy your favorite tea, but like everything else, drink it in moderation."
Saturday, July 10, 2010
Jon's Health Tips - Latest Health Research
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Lots of news the last two weeks, including big reports questioning the value of aspirin, antioxidants, statins and alcohol. At least alcohol was endorsed!
Here we go:
It’s a good thing I don’t relax too much:
Mild stress might by itself curb cancer growth.
I don’t take fish oil supplements on days I eat fish, but I am reconsidering that now:
Fish oil may reduce risk of breast cancer
More good news about Vitamin D – I need to keep up my supplement intake even in summer:
Low vitamin D linked to the metabolic syndrome in elderly people
Vitamin D Receptor Emerges as a Key Player in ‘Gut Flora’
I still believe strongly in the efficacy of aspirin, which I take regularly:
Benefits For Healthy People Of Aspirin Questioned
And I still believe that antioxidants, especially in food, are essential to good health and a long life:
Antioxidants don’t help?
But I also take coenzyme Q10:
Antioxidants do help arteries stay healthy
I’m holding steady on eating dark chocolate every day (at last no one is questioning that yet):
Dark chocolate lowers blood pressure
Cocoa flavanols improve vascular and blood pressure measures for coronary artery disease patients
I wish I had the energy to do more cycling (but soccer 3 times a week and kayaking are too much out of me, not to mention my actual work):
Health Benefits of Urban Cycling Outweigh Risks
I’m still taking Red Yeast Rice but will begin a real statin soon, just as the evidence seems to weigh in against it:
Do statins prevent death in high-risk individuals without heart disease?
And if that news weren’t depressing enough:
Link between statin drugs and depression
But:
Statins associated with lower cancer recurrence following prostatectomy
I tried beetroot juice but I almost threw up:
Beetroot juice lowers blood pressure
I need to eat more broccoli ( I hate Brussels sprouts):
Broccoli and Brussels sprouts fight cancer
I knew there was a good reason to drink lots of green tea before each of my soccer games:
Caffeine boosts performance
I would like to be able to drink two glasses of red wine a day, but usually manage only one, and sometimes substitute beer:
Examining cognitive risks and benefits of alcohol consumption
“Most studies suggest less decline in cognitive functioning over time, and lower risk of dementia, among moderate drinkers in comparison with non-drinkers. “
and of course I am a big believer in exercise, (although not while drinking):
Physical activity reduces risk of cognitive impairment in later life
Maybe I should add olive oil to my daily oatmeal?
Virgin olive oil and a Mediterranean diet fight heart disease
Virgin olive oil protects against breast cancer
Lots of news the last two weeks, including big reports questioning the value of aspirin, antioxidants, statins and alcohol. At least alcohol was endorsed!
Here we go:
It’s a good thing I don’t relax too much:
Mild stress might by itself curb cancer growth.
"Living in an environment rich with physical, mental and social stimulation – a setting that causes mild stress – might by itself curb cancer growth."
I don’t take fish oil supplements on days I eat fish, but I am reconsidering that now:
Fish oil may reduce risk of breast cancer
“This research is the first to demonstrate a link between the use of fish oil supplements and a reduction in breast cancer. Studies of dietary intake of fish or omega-3 fatty acids have not been consistent. It may be that the amount of omega-3 fatty acids in fish oil supplements are higher than most people would typically get from their diet. Fish oil continues to excite many, as evidence emerges about its protective effect on cardiovascular disease and now cancer."
More good news about Vitamin D – I need to keep up my supplement intake even in summer:
Low vitamin D linked to the metabolic syndrome in elderly people
Vitamin D Receptor Emerges as a Key Player in ‘Gut Flora’
“Vitamin D deficiency is a known factor in the pathology of inflammatory bowel disease and colon cancer,” said microbiologist Jun Sun, Ph.D., of the University of Rochester Medical Center, “but there have been very few reports about how bacteria might play a role by targeting the vitamin D receptor. Our work suggests one possible mechanism, by working through the vitamin D receptor, a sensor and regulator for the majority of functions of vitamin D.” (Funny name for a Vitamin D researcher!)
I still believe strongly in the efficacy of aspirin, which I take regularly:
Benefits For Healthy People Of Aspirin Questioned
“While it is known that aspirin prevents heart attacks and strokes in people with established heart disease—benefits which clearly outweigh any risks associated with aspirin, such as bleeding—the role of aspirin in people without a history of cardiovascular disease is less certain.”
And I still believe that antioxidants, especially in food, are essential to good health and a long life:
Antioxidants don’t help?
“Don't put down the red wine and vitamins just yet, but if you're taking antioxidants because you hope to live longer, consider this: a new study casts doubt on the theory that oxidative stress to our tissues shortens lifespan.”
But I also take coenzyme Q10:
Antioxidants do help arteries stay healthy
“Long-term supplementation with dietary antioxidants has beneficial effects on sugar and fat metabolism, blood pressure and arterial flexibility in patients with multiple cardiovascular risk factors. Researchers report these positive results in a randomized controlled trial of combined vitamin C, vitamin E, coenzyme Q10 and selenium capsules.”
I’m holding steady on eating dark chocolate every day (at last no one is questioning that yet):
Dark chocolate lowers blood pressure
Cocoa flavanols improve vascular and blood pressure measures for coronary artery disease patients
“Flavanols are phytonutrient compounds that are found naturally in apples, grapes, tea, cocoa and cherries, which account for the antioxidant effect provided by red wine and green tea. The study found a protective effect from a cocoa drink with 375 mg of flavanols, but according to researchers, a standard or recommended dosage has not yet been defined to achieve optimal health benefit.”
I wish I had the energy to do more cycling (but soccer 3 times a week and kayaking are too much out of me, not to mention my actual work):
Health Benefits of Urban Cycling Outweigh Risks
“Health benefits from cycling may also vary by the age. For example, older, sedentary adults tend to benefit most from increased exercise. However, benefits of exercise can be substantial for persons of all ages; some researchers estimate that inactive individuals who begin moderate exercise programs can lower their risk of death from all causes by 10% to 50%.”
I’m still taking Red Yeast Rice but will begin a real statin soon, just as the evidence seems to weigh in against it:
Do statins prevent death in high-risk individuals without heart disease?
“A meta-analysis of previously published studies finds no evidence that statins are associated with a reduced risk of death among individuals at risk for but with no history of cardiovascular disease, Statins are now one of the most widely used drugs for the treatment and prevention of cardiovascular disease both among individuals with established disease and among high-risk healthy individuals who are at elevated risk of incident [new-onset] cardiovascular disease.
"There is little debate that, compared with placebo, statin therapy among individuals with established coronary heart disease not only prevents complications related to atherosclerosis but also reduces all-cause mortality [death]." However, there is little evidence that statins reduce the risk of dying from any cause in individuals without heart disease. This, along with harms caused by statins in some subgroups, have called into question the benefit of statins in primary prevention (prevention of the development of heart disease)."
And if that news weren’t depressing enough:
Link between statin drugs and depression
“Scientists are reporting a possible explanation for the symptoms of anxiety and depression that occur in some patients taking the popular statin family of anti-cholesterol drugs, and reported by some individuals on low-cholesterol diets. These symptoms could result from long-term, low levels of cholesterol in the brain.”
But:
Statins associated with lower cancer recurrence following prostatectomy
I tried beetroot juice but I almost threw up:
Beetroot juice lowers blood pressure
I need to eat more broccoli ( I hate Brussels sprouts):
Broccoli and Brussels sprouts fight cancer
I knew there was a good reason to drink lots of green tea before each of my soccer games:
Caffeine boosts performance
"A very high dosage of caffeine, most likely achieved via tablets, powder or a concentrated liquid, is feasible and might prove attractive to a number of athletes wishing to improve their athletic performance"
I would like to be able to drink two glasses of red wine a day, but usually manage only one, and sometimes substitute beer:
Examining cognitive risks and benefits of alcohol consumption
“Most studies suggest less decline in cognitive functioning over time, and lower risk of dementia, among moderate drinkers in comparison with non-drinkers. “
and of course I am a big believer in exercise, (although not while drinking):
Physical activity reduces risk of cognitive impairment in later life
Women who are physically active at any point over the life course (teenage, age 30, age 50, late life) have lower risk of cognitive impairment in late-life compared to those who are inactive, but teenage physical activity appears to be most important.
Maybe I should add olive oil to my daily oatmeal?
Virgin olive oil and a Mediterranean diet fight heart disease
“Everyone knows olive oil and a Mediterranean diet are associated with a lower risk for cardiovascular disease, but a new research report offers a surprising reason why: These foods change how genes associated with atherosclerosis function.”
Virgin olive oil protects against breast cancer
Thursday, July 8, 2010
Stress of an enriched environment might curb cancer growth
Ω
Living in an environment rich with physical, mental and social stimulation – a setting that causes mild stress – might by itself curb cancer growth, according to a new study led by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute.
The animal study, published in the July 9 issue of the journal Cell, also shows how this effect happens and that it might have therapeutic use.
The researchers discovered that an enriched environment activates a nervous-system pathway by which the brain talks to fat tissue. That pathway, called the hypothalamic-sympathoneural-adipocyte (HSA) axis tells fat cells to stop releasing a hormone called leptin into the bloodstream. Leptin normally helps restrain appetite, but this study discovered that it also accelerates cancer growth.
The enriched environment had the same cancer-curbing influence in models of melanoma and colon cancer.
"People tend to think that cancer survivors should avoid stress, but our data suggests that this is not completely true," says research leader Dr. Matthew J. During, professor of neuroscience, of neurological surgery and of molecular virology, immunology and medical genetics.
"The anti-cancer effect we observed in this study was not due simply to increased activity by the animals, but rather it was induced by social and physical challenges that are associated with the release of stress hormones from the adrenal gland.
"But the most dramatic hormonal change we observed was the drop in leptin from fat after richer housing conditions activated the HSA pathway. That pathway is also present in humans, where it is likely to be activated by a more complex and challenging life," he adds.
The enriched environment created for this study housed 20 mice in large containers equipped with toys, hiding places and running wheels, along with unlimited food and water. Control mice were housed in groups of five in smaller, standard laboratory containers with no toys but with unlimited food and water.
The researchers injected human melanoma cells under the skin in both sets of animals. After three weeks of enriched housing, mice had tumors that were about half the size of those in control mice. With six weeks of enrichment, those tumors were 80 percent smaller than those in control animals, and almost 20 percent of the animals in the enriched group had no visible tumors at all. Control animals, on the other hand, all had visible tumors.
Investigating this effect further, During and his colleagues looked for changes in several metabolic hormones in the blood. Of those, leptin showed a dramatic drop in the enriched group.
A series of experiments demonstrated that leptin and the nervous system pathway really did influence tumor growth. Blocking the hormone altogether, for example, mimicked the enriched-environment effect, and the animals developed smaller tumors.
Looking closely at the region of the brain called the hypothalamus, the researchers found that a gene called BDNF, which plays an important role in controlling food intake and energy balance, was much more active in the enriched group.
Transplanting extra copies of this gene into the hypothalamus of mice in standard housing mimicked the effects of the enriched environment and reduced the size of the tumors in these animals by 75 percent. Blocking the gene, on the other hand, cancelled this effect and caused even enriched animals to develop large tumors.
"This is the first time anyone has shown that putting a single gene into the brain could have an impact on peripheral cancer," During says.
Next, the researchers studied a strain of mice that was unable to make leptin and so lacked the hormone altogether. Infusing these animals with leptin, however, caused them to develop melanoma tumors that were 40 percent larger than those in similar animals infused with a saline solution.
Finally, an enriched environment had a similar cancer-controlling effect in both of two colon-cancer models. In one of these, tumors develop spontaneously in the intestine; in the other, visible tumors develop after cancer cells are injected under the skin.
Using the second model, researchers discovered that the anti-cancer effect occurred when animals were placed in the enriched environment after visible tumors were well established.
"This finding suggests that such an enriched environment might have therapeutic importance," During says.
During notes that increased physical activity – running in a wheel – alone did not produce the anti-cancer effect or activate the HSA axis. In contrast, increased activity reduced levels of the stress hormone corticosterone in control animals, whereas levels of this stress hormone rose in animals in enriched housing, an outcome likely due to the challenges and social conflicts associated with larger and more complex group housing.
"Overall, our study suggests that an environmental or genetic activation of this nervous system pathway leads to a marked drop in serum leptin levels, and that this inhibits tumor growth."
Living in an environment rich with physical, mental and social stimulation – a setting that causes mild stress – might by itself curb cancer growth, according to a new study led by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute.
The animal study, published in the July 9 issue of the journal Cell, also shows how this effect happens and that it might have therapeutic use.
The researchers discovered that an enriched environment activates a nervous-system pathway by which the brain talks to fat tissue. That pathway, called the hypothalamic-sympathoneural-adipocyte (HSA) axis tells fat cells to stop releasing a hormone called leptin into the bloodstream. Leptin normally helps restrain appetite, but this study discovered that it also accelerates cancer growth.
The enriched environment had the same cancer-curbing influence in models of melanoma and colon cancer.
"People tend to think that cancer survivors should avoid stress, but our data suggests that this is not completely true," says research leader Dr. Matthew J. During, professor of neuroscience, of neurological surgery and of molecular virology, immunology and medical genetics.
"The anti-cancer effect we observed in this study was not due simply to increased activity by the animals, but rather it was induced by social and physical challenges that are associated with the release of stress hormones from the adrenal gland.
"But the most dramatic hormonal change we observed was the drop in leptin from fat after richer housing conditions activated the HSA pathway. That pathway is also present in humans, where it is likely to be activated by a more complex and challenging life," he adds.
The enriched environment created for this study housed 20 mice in large containers equipped with toys, hiding places and running wheels, along with unlimited food and water. Control mice were housed in groups of five in smaller, standard laboratory containers with no toys but with unlimited food and water.
The researchers injected human melanoma cells under the skin in both sets of animals. After three weeks of enriched housing, mice had tumors that were about half the size of those in control mice. With six weeks of enrichment, those tumors were 80 percent smaller than those in control animals, and almost 20 percent of the animals in the enriched group had no visible tumors at all. Control animals, on the other hand, all had visible tumors.
Investigating this effect further, During and his colleagues looked for changes in several metabolic hormones in the blood. Of those, leptin showed a dramatic drop in the enriched group.
A series of experiments demonstrated that leptin and the nervous system pathway really did influence tumor growth. Blocking the hormone altogether, for example, mimicked the enriched-environment effect, and the animals developed smaller tumors.
Looking closely at the region of the brain called the hypothalamus, the researchers found that a gene called BDNF, which plays an important role in controlling food intake and energy balance, was much more active in the enriched group.
Transplanting extra copies of this gene into the hypothalamus of mice in standard housing mimicked the effects of the enriched environment and reduced the size of the tumors in these animals by 75 percent. Blocking the gene, on the other hand, cancelled this effect and caused even enriched animals to develop large tumors.
"This is the first time anyone has shown that putting a single gene into the brain could have an impact on peripheral cancer," During says.
Next, the researchers studied a strain of mice that was unable to make leptin and so lacked the hormone altogether. Infusing these animals with leptin, however, caused them to develop melanoma tumors that were 40 percent larger than those in similar animals infused with a saline solution.
Finally, an enriched environment had a similar cancer-controlling effect in both of two colon-cancer models. In one of these, tumors develop spontaneously in the intestine; in the other, visible tumors develop after cancer cells are injected under the skin.
Using the second model, researchers discovered that the anti-cancer effect occurred when animals were placed in the enriched environment after visible tumors were well established.
"This finding suggests that such an enriched environment might have therapeutic importance," During says.
During notes that increased physical activity – running in a wheel – alone did not produce the anti-cancer effect or activate the HSA axis. In contrast, increased activity reduced levels of the stress hormone corticosterone in control animals, whereas levels of this stress hormone rose in animals in enriched housing, an outcome likely due to the challenges and social conflicts associated with larger and more complex group housing.
"Overall, our study suggests that an environmental or genetic activation of this nervous system pathway leads to a marked drop in serum leptin levels, and that this inhibits tumor growth."
Fish oil may reduce risk of breast cancer
Ω
A recent report in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, adds to the growing evidence that fish oil supplements may play a role in preventing chronic disease.
Researchers at the Fred Hutchinson Cancer Research Center in Seattle, Wash., led by Emily White, Ph.D., a member of the public health sciences division, asked 35,016 postmenopausal women who did not have a history of breast cancer to complete a 24-page questionnaire about their use of non-vitamin, non-mineral "specialty" supplements in the Vitamins and Lifestyle (VITAL) cohort study.
After six years of follow-up, 880 cases of breast cancer were identified using the Surveillance, Epidemiology and End Results registry.
Regular use of fish oil supplements, which contain high levels of the omega-3 fatty acids, EPA and DHA, was linked with a 32 percent reduced risk of breast cancer. The reduction in risk appeared to be restricted to invasive ductal breast cancer, the most common type of the disease.
The use of other specialty supplements, many of which are commonly taken by women to treat symptoms of menopause, was not associated with breast cancer risk.
This research is the first to demonstrate a link between the use of fish oil supplements and a reduction in breast cancer. Studies of dietary intake of fish or omega-3 fatty acids have not been consistent.
"It may be that the amount of omega-3 fatty acids in fish oil supplements are higher than most people would typically get from their diet," White said.
However, White cautioned against gleaning any recommendations from the results of one study.
"Without confirming studies specifically addressing this," she said, "we should not draw any conclusions about a causal relationship."
Edward Giovannucci, M.D., Sc.D., professor of nutrition and epidemiology at the Harvard School of Public Health and an editorial board member of Cancer Epidemiology, Biomarkers & Prevention, agreed.
"It is very rare that a single study should be used to make a broad recommendation," said Giovannucci. "Over a period of time, as the studies confirm each other, we can start to make recommendations."
Still, fish oil continues to excite many, as evidence emerges about its protective effect on cardiovascular disease and now cancer.
Harvard researchers are currently enrolling patients for the randomized Vitamin D and Omega-3 Trial (also called VITAL), which will assess the impact of fish oil supplements and vitamin D on cancer, heart disease and stroke.
The researchers plan to enroll 20,000 U.S. men aged 60 years and older and women aged 65 years and older who do not have a history of these diseases and have never taken supplements.
A recent report in Cancer Epidemiology, Biomarkers & Prevention, a journal of the American Association for Cancer Research, adds to the growing evidence that fish oil supplements may play a role in preventing chronic disease.
Researchers at the Fred Hutchinson Cancer Research Center in Seattle, Wash., led by Emily White, Ph.D., a member of the public health sciences division, asked 35,016 postmenopausal women who did not have a history of breast cancer to complete a 24-page questionnaire about their use of non-vitamin, non-mineral "specialty" supplements in the Vitamins and Lifestyle (VITAL) cohort study.
After six years of follow-up, 880 cases of breast cancer were identified using the Surveillance, Epidemiology and End Results registry.
Regular use of fish oil supplements, which contain high levels of the omega-3 fatty acids, EPA and DHA, was linked with a 32 percent reduced risk of breast cancer. The reduction in risk appeared to be restricted to invasive ductal breast cancer, the most common type of the disease.
The use of other specialty supplements, many of which are commonly taken by women to treat symptoms of menopause, was not associated with breast cancer risk.
This research is the first to demonstrate a link between the use of fish oil supplements and a reduction in breast cancer. Studies of dietary intake of fish or omega-3 fatty acids have not been consistent.
"It may be that the amount of omega-3 fatty acids in fish oil supplements are higher than most people would typically get from their diet," White said.
However, White cautioned against gleaning any recommendations from the results of one study.
"Without confirming studies specifically addressing this," she said, "we should not draw any conclusions about a causal relationship."
Edward Giovannucci, M.D., Sc.D., professor of nutrition and epidemiology at the Harvard School of Public Health and an editorial board member of Cancer Epidemiology, Biomarkers & Prevention, agreed.
"It is very rare that a single study should be used to make a broad recommendation," said Giovannucci. "Over a period of time, as the studies confirm each other, we can start to make recommendations."
Still, fish oil continues to excite many, as evidence emerges about its protective effect on cardiovascular disease and now cancer.
Harvard researchers are currently enrolling patients for the randomized Vitamin D and Omega-3 Trial (also called VITAL), which will assess the impact of fish oil supplements and vitamin D on cancer, heart disease and stroke.
The researchers plan to enroll 20,000 U.S. men aged 60 years and older and women aged 65 years and older who do not have a history of these diseases and have never taken supplements.
Wednesday, July 7, 2010
High blood levels of vitamin E reduces risk of Alzheimer's
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High levels of several vitamin E components in the blood are associated with a decreased risk for Alzheimer's disease (AD) in advanced age, suggesting that vitamin E may help prevent cognitive deterioration in elderly people. This is the conclusion reached in a Swedish study published in the July 2010 issue of the Journal of Alzheimer s Disease.
"Vitamin E is a family of eight natural components, but most studies related to Alzheimer s disease investigate only one of these components, ±-tocopherol", says Dr. Francesca Mangialasche, who led the study. "We hypothesized that all the vitamin E family members could be important in protecting against AD. If confirmed, this result has implications for both individuals and society, as 70 percent of all dementia cases in the general population occur in people over 75 years of age, and the study suggests a protective effect of vitamin E against AD in individuals aged 80+."
The study was conducted at the Aging Research Center (ARC), Karolinska Institutet, Stockholm, Sweden, in collaboration with the Institute of Gerontology and Geriatrics, University of Perugia, Italy. The study included a sample of 232 participants from the Kungsholmen Project, a population-based longitudinal study on aging and dementia in Stockholm (Kungsholmen parish). All participants were aged 80+ years and were dementia-free at the beginning of the study (baseline). After 6-years of follow-up, 57 AD cases were identified.
The blood levels of all eight natural vitamin E components were measured at the beginning of the study. Subjects with higher blood levels (highest tertile) were compared with subjects who had lower blood levels (lowest tertile) to verify whether these two groups developed dementia at different rates. The study found that subjects with higher blood levels of all the vitamin E family forms had a reduced risk of developing AD, compared to subjects with lower levels. After adjusting for various confounders, the risk was reduced by 45-54%, depending on the vitamin E component.
Dr Mangialasche notes that the protective effect of vitamin E seems to be related to the combination of the different forms. Another recent study indicated that supplements containing high doses of the E vitamin form ±-tocopherol may increase mortality, emphasizing that such dietary supplements, if not used in a balanced way, may be more harmful than previously thought.
"Elderly people as a group are large consumers of vitamin E supplements, which usually contain only ±-tocopherol, and this often at high doses", says Dr Mangialasche. "Our findings need to be confirmed by other studies, but they open up for the possibility that the balanced presence of different vitamin E forms can have an important neuroprotective effect."
High levels of several vitamin E components in the blood are associated with a decreased risk for Alzheimer's disease (AD) in advanced age, suggesting that vitamin E may help prevent cognitive deterioration in elderly people. This is the conclusion reached in a Swedish study published in the July 2010 issue of the Journal of Alzheimer s Disease.
"Vitamin E is a family of eight natural components, but most studies related to Alzheimer s disease investigate only one of these components, ±-tocopherol", says Dr. Francesca Mangialasche, who led the study. "We hypothesized that all the vitamin E family members could be important in protecting against AD. If confirmed, this result has implications for both individuals and society, as 70 percent of all dementia cases in the general population occur in people over 75 years of age, and the study suggests a protective effect of vitamin E against AD in individuals aged 80+."
The study was conducted at the Aging Research Center (ARC), Karolinska Institutet, Stockholm, Sweden, in collaboration with the Institute of Gerontology and Geriatrics, University of Perugia, Italy. The study included a sample of 232 participants from the Kungsholmen Project, a population-based longitudinal study on aging and dementia in Stockholm (Kungsholmen parish). All participants were aged 80+ years and were dementia-free at the beginning of the study (baseline). After 6-years of follow-up, 57 AD cases were identified.
The blood levels of all eight natural vitamin E components were measured at the beginning of the study. Subjects with higher blood levels (highest tertile) were compared with subjects who had lower blood levels (lowest tertile) to verify whether these two groups developed dementia at different rates. The study found that subjects with higher blood levels of all the vitamin E family forms had a reduced risk of developing AD, compared to subjects with lower levels. After adjusting for various confounders, the risk was reduced by 45-54%, depending on the vitamin E component.
Dr Mangialasche notes that the protective effect of vitamin E seems to be related to the combination of the different forms. Another recent study indicated that supplements containing high doses of the E vitamin form ±-tocopherol may increase mortality, emphasizing that such dietary supplements, if not used in a balanced way, may be more harmful than previously thought.
"Elderly people as a group are large consumers of vitamin E supplements, which usually contain only ±-tocopherol, and this often at high doses", says Dr Mangialasche. "Our findings need to be confirmed by other studies, but they open up for the possibility that the balanced presence of different vitamin E forms can have an important neuroprotective effect."
Vitamin D Receptor Emerges as a Key Player in ‘Gut Flora’
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Within the human digestive tract is a teeming mass of hundreds of types of bacteria, a potpourri of microbes numbering in the trillions that help us digest food and keep bad bacteria in check.
Now scientists have found that the vitamin D receptor is a key player amid the gut bacteria – what scientists refer to matter-of-factly as the “gut flora” – helping to govern their activity, responding to their cues, and sometimes countering their presence. The work was published online recently in the American Journal of Pathology.
The findings deliver a new lead to scientists investigating how bacteria might play a role in the development of inflammatory bowel diseases such as Crohn’s disease or ulceractive colitis. The work complements studies suggesting that Salmonella infection can increase the risk of inflammatory bowel disease.
“Vitamin D deficiency is a known factor in the pathology of inflammatory bowel disease and colon cancer,” said microbiologist Jun Sun, Ph.D., of the University of Rochester Medical Center, “but there have been very few reports about how bacteria might play a role by targeting the vitamin D receptor. Our work suggests one possible mechanism, by working through the vitamin D receptor, a sensor and regulator for the majority of functions of vitamin D.”
Sun specializes in the actions of bacteria in the body and how their interactions within the body contribute to disease. She has shown that bacteria often found in the human intestine affect molecular signals known to contribute to inflammatory response and cell growth.
Shaoping Wu, Ph.D.
Her work with the vitamin D receptor takes place at a time when the molecule is coming under increasing scrutiny. Scientists have associated vitamin D and the receptor with many types of cancer, as well as osteoporosis, heart disease, diabetes, inflammatory bowel disease, and infection.
Sun’s team took a close look at the vitamin D receptor in mice and its interactions with bacteria in the colon. The team studied normal mice; mice in which the vitamin D receptor had been knocked out; and mice that were completely free of any germs. Scientists observed how the mice responded to infection with either a harmless strain of E. coli or a pathogenic strain of Salmonella Typhimurium.
The team found that Salmonella is able to regulate the vitamin D receptor, increasing its activity and determining where in the colon the receptor is active. In the presence of Salmonella, the receptor was more prevalent than usual deep within folded intestinal structures known as crypts.
Sun’s team also discovered that the vitamin D receptor plays a key role in defending the body from assault by Salmonella and squelching inflammation. The receptor stops a molecule known as NF-Kappa B, a well-known master player in the world of inflammation, by binding to it and preventing it from activating other inflammatory molecules. While scientists have known that the receptor interacts with NF-Kappa B, details of the interaction modulated by bacteria in the colon are new.
The scientists found that Salmonella was much more virulent and aggressive in mice in which the vitamin D receptor had been turned off. These mice showed higher levels of activity of inflammatory molecules, and they lost weight more quickly and were much more likely to die in response to infection.
“We live together in a mutually beneficial state with most of the bacteria in our gut,” said Sun, assistant professor in the Gastroenterology and Hepatology Division of the Department of Medicine. “They help us digest foods like fruits and vegetables, and we provide them a place to live and thrive. We co-exist peacefully – most of the time.
“But we aren’t able to culture most of these bacteria in the laboratory, and we don’t know what most of them are doing. We need to understand our gut flora much more than we do. This is particularly important for understanding how we might manipulate the natural gut flora to stop an invader like Salmonella,” added Sun, who also has appointments in the James P. Wilmot Cancer Center and the Department of Microbiology and Immunology.
Within the human digestive tract is a teeming mass of hundreds of types of bacteria, a potpourri of microbes numbering in the trillions that help us digest food and keep bad bacteria in check.
Now scientists have found that the vitamin D receptor is a key player amid the gut bacteria – what scientists refer to matter-of-factly as the “gut flora” – helping to govern their activity, responding to their cues, and sometimes countering their presence. The work was published online recently in the American Journal of Pathology.
The findings deliver a new lead to scientists investigating how bacteria might play a role in the development of inflammatory bowel diseases such as Crohn’s disease or ulceractive colitis. The work complements studies suggesting that Salmonella infection can increase the risk of inflammatory bowel disease.
“Vitamin D deficiency is a known factor in the pathology of inflammatory bowel disease and colon cancer,” said microbiologist Jun Sun, Ph.D., of the University of Rochester Medical Center, “but there have been very few reports about how bacteria might play a role by targeting the vitamin D receptor. Our work suggests one possible mechanism, by working through the vitamin D receptor, a sensor and regulator for the majority of functions of vitamin D.”
Sun specializes in the actions of bacteria in the body and how their interactions within the body contribute to disease. She has shown that bacteria often found in the human intestine affect molecular signals known to contribute to inflammatory response and cell growth.
Shaoping Wu, Ph.D.
Her work with the vitamin D receptor takes place at a time when the molecule is coming under increasing scrutiny. Scientists have associated vitamin D and the receptor with many types of cancer, as well as osteoporosis, heart disease, diabetes, inflammatory bowel disease, and infection.
Sun’s team took a close look at the vitamin D receptor in mice and its interactions with bacteria in the colon. The team studied normal mice; mice in which the vitamin D receptor had been knocked out; and mice that were completely free of any germs. Scientists observed how the mice responded to infection with either a harmless strain of E. coli or a pathogenic strain of Salmonella Typhimurium.
The team found that Salmonella is able to regulate the vitamin D receptor, increasing its activity and determining where in the colon the receptor is active. In the presence of Salmonella, the receptor was more prevalent than usual deep within folded intestinal structures known as crypts.
Sun’s team also discovered that the vitamin D receptor plays a key role in defending the body from assault by Salmonella and squelching inflammation. The receptor stops a molecule known as NF-Kappa B, a well-known master player in the world of inflammation, by binding to it and preventing it from activating other inflammatory molecules. While scientists have known that the receptor interacts with NF-Kappa B, details of the interaction modulated by bacteria in the colon are new.
The scientists found that Salmonella was much more virulent and aggressive in mice in which the vitamin D receptor had been turned off. These mice showed higher levels of activity of inflammatory molecules, and they lost weight more quickly and were much more likely to die in response to infection.
“We live together in a mutually beneficial state with most of the bacteria in our gut,” said Sun, assistant professor in the Gastroenterology and Hepatology Division of the Department of Medicine. “They help us digest foods like fruits and vegetables, and we provide them a place to live and thrive. We co-exist peacefully – most of the time.
“But we aren’t able to culture most of these bacteria in the laboratory, and we don’t know what most of them are doing. We need to understand our gut flora much more than we do. This is particularly important for understanding how we might manipulate the natural gut flora to stop an invader like Salmonella,” added Sun, who also has appointments in the James P. Wilmot Cancer Center and the Department of Microbiology and Immunology.
Tuesday, July 6, 2010
Benefits For Healthy People Of Aspirin Questioned
Aspirin is one of the most commonly used medicines in the world. Whether the benefits of taking aspirin to maintain a life free of disability in an older person outweigh the risk of bleeding is a critically important health question to answer.
While it is known that aspirin prevents heart attacks and strokes in people with established heart disease—benefits which clearly outweigh any risks associated with aspirin, such as bleeding—the role of aspirin in people without a history of cardiovascular disease is less certain.
To date, very little information is available about the overall effects of aspirin in older adults, because most trials focus on middle-aged people.
Because of its proven effectiveness in preventing second events, many doctors have also prescribed aspirin to prevent heart attacks and strokes in otherwise healthy people/. However, in the last couple of years, serious doubts have been raised about the evidence supporting this practice, and as a result, editorials in major medical journals have called for this question to be settled.
While it is known that aspirin prevents heart attacks and strokes in people with established heart disease—benefits which clearly outweigh any risks associated with aspirin, such as bleeding—the role of aspirin in people without a history of cardiovascular disease is less certain.
To date, very little information is available about the overall effects of aspirin in older adults, because most trials focus on middle-aged people.
Because of its proven effectiveness in preventing second events, many doctors have also prescribed aspirin to prevent heart attacks and strokes in otherwise healthy people/. However, in the last couple of years, serious doubts have been raised about the evidence supporting this practice, and as a result, editorials in major medical journals have called for this question to be settled.
Antioxidants do help arteries stay healthy
Ω
Long-term supplementation with dietary antioxidants has beneficial effects on sugar and fat metabolism, blood pressure and arterial flexibility in patients with multiple cardiovascular risk factors. Researchers writing in BioMed Central's open access journal Nutrition and Metabolism report these positive results in a randomized controlled trial of combined vitamin C, vitamin E, coenzyme Q10 and selenium capsules.
Reuven Zimlichman worked with a team of researchers from Wolfson Medical Center, Israel, to carry out the study in 70 patients from the centre's hypertension clinic. He said, "Antioxidant supplementation significantly increased large and small artery elasticity in patients with multiple cardiovascular risk factors. This beneficial vascular effect was associated with an improvement in glucose and lipid metabolism as well as significant decrease in blood pressure".
Previous results from clinical trials into the cardiovascular health effects of antioxidants have been equivocal. In order to shed more light onto the matter, Zimlichman and his colleagues randomised the 70 patients to receive either antioxidants or placebo capsules for six months. Tests at the beginning of the trial, after three months and at the six month mark revealed that the patients in the antioxidant group had more elastic arteries (a measure of increased cardiovascular health) and better blood sugar and cholesterol profiles. According to Zimlichman, "The findings of the present study justify investigating the overall clinical impact of antioxidant treatment in patients with multiple cardiovascular risk factors".
1. Effect of long-term treatment with antioxidants (vitamin C, vitamin E, coenzyme Q10 and selenium) on arterial compliance, humoral factors and inflammatory markers in patients with multiple cardiovascular risk factors.
Long-term supplementation with dietary antioxidants has beneficial effects on sugar and fat metabolism, blood pressure and arterial flexibility in patients with multiple cardiovascular risk factors. Researchers writing in BioMed Central's open access journal Nutrition and Metabolism report these positive results in a randomized controlled trial of combined vitamin C, vitamin E, coenzyme Q10 and selenium capsules.
Reuven Zimlichman worked with a team of researchers from Wolfson Medical Center, Israel, to carry out the study in 70 patients from the centre's hypertension clinic. He said, "Antioxidant supplementation significantly increased large and small artery elasticity in patients with multiple cardiovascular risk factors. This beneficial vascular effect was associated with an improvement in glucose and lipid metabolism as well as significant decrease in blood pressure".
Previous results from clinical trials into the cardiovascular health effects of antioxidants have been equivocal. In order to shed more light onto the matter, Zimlichman and his colleagues randomised the 70 patients to receive either antioxidants or placebo capsules for six months. Tests at the beginning of the trial, after three months and at the six month mark revealed that the patients in the antioxidant group had more elastic arteries (a measure of increased cardiovascular health) and better blood sugar and cholesterol profiles. According to Zimlichman, "The findings of the present study justify investigating the overall clinical impact of antioxidant treatment in patients with multiple cardiovascular risk factors".
1. Effect of long-term treatment with antioxidants (vitamin C, vitamin E, coenzyme Q10 and selenium) on arterial compliance, humoral factors and inflammatory markers in patients with multiple cardiovascular risk factors.
Cocoa flavanols improve vascular and blood pressure measures for coronary artery disease patients
Ω
A new study by UCSF cardiologists and researchers found that high concentrations of cocoa flavanols decrease blood pressure, improve the health of blood vessels and increase the number of circulating blood-vessel-forming cells in patients with heart disease. The findings indicate that foods rich in flavanols – such as cocoa products, tea, wine, and various fruits and vegetables – have a cardio-protective benefit for heart disease patients.
Findings will be published online July 5th and in the July 13, 2010 issue of the Journal of the American College of Cardiology (JACC).
Flavanols are phytonutrient compounds that are found naturally in apples, grapes, tea, cocoa and cherries, which account for the antioxidant effect provided by red wine and green tea. The study found a protective effect from a cocoa drink with 375 mg of flavanols, but according to researchers, a standard or recommended dosage has not yet been defined to achieve optimal health benefit.
The UCSF team has shown for the first time that one of the possible mechanisms of flavanol's benefit is an increase in the circulation of so-called angiogenic cells in the blood. These cells, also known as early endothelial progenitor cells, are critical for the repair process after vascular injury, and perform function and maintenance roles in the endothelium. Endothelium is the thin layer of cells that line the interior wall of blood vessels.
"Reduced blood vessel function is a hallmark of early development of coronary artery disease," said cardiologist Yerem Yeghiazarians, MD, senior author, associate professor of medicine, and researcher in the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. "If we can improve the health and function of damaged blood vessels, heart disease patients will have a better chance of survival."
In 2005, researchers reported that an increased level of circulating angiogenic cells is associated with a decreased risk of death from cardiovascular causes (New England Journal of Medicine by Werner, N., et al.)
In the current study, the benefit seen from the two-fold increase in circulating angiogenic cells was similar to that achieved by therapy with statins and with lifestyle changes such as exercise and smoking cessation. The benefit demonstrated with cocoa flavanol therapy occurred in addition to the medical regimen already being taken by study participants.
"Our data support the concept that dietary flavanols at the levels provided - in tandem with current medical therapy - are safe, improve cardiovascular function, and increase circulating angiogenic cells, which have previously been shown to correlate positively with long-term cardiovascular outcomes" said Yeghiazarians. "Long-term trials examining the effects of high-flavanol diets on cardiovascular health and function are warranted, but these early findings help us understand how these compounds impact the function of damaged blood vessels."
The study included 16 coronary artery disease patients aged 64 years (±three years) who received a high-flavanol cocoa drink (containing 375 mg of flavanols) twice a day over 30 days and then a nutrient-matched low-flavanol cocoa drink (containing 9mg flavanols) twice a day over 30 days.
The study was randomized, controlled and "masked", meaning both the doctors and patients were prevented from knowing which variation of the cocoa drink a patient was drinking at a given time until after the study was completed. The patients continued taking all regular medications for their underlying heart disease during the study period, including statin medications for lowering the cholesterol levels to recommended goals.
Researchers calculated the outcome of the cocoa intervention using blood pressure readings, ultrasound to measure dilation of the brachial artery, and cell assays to calculate the number and behavior of circulating angiogenic cells. The tests showed a 47 percent improvement in vasodilation, or widening rather than constriction, of the brachial artery in the high-flavanol time period compared to the low-flavanol period. In addition, circulating angiogenic cells increased 2.2-fold and systolic blood pressure decreased among the high-flavanol versus low-flavanol periods.
"This is exciting data," Yeghiazarians added. "Our findings demonstrate that a further increase in endothelial function and improvement in blood pressure can be achieved by complementing standard treatment with a flavanol-rich diet. The 80 million Americans impacted by heart disease may be glad to hear this." Notably, the therapy did not influence fasting glucose levels of study participants. (Fasting glucose is the standard for measuring an individual's blood sugar level to diagnose conditions such as diabetes and heart disease).
A new study by UCSF cardiologists and researchers found that high concentrations of cocoa flavanols decrease blood pressure, improve the health of blood vessels and increase the number of circulating blood-vessel-forming cells in patients with heart disease. The findings indicate that foods rich in flavanols – such as cocoa products, tea, wine, and various fruits and vegetables – have a cardio-protective benefit for heart disease patients.
Findings will be published online July 5th and in the July 13, 2010 issue of the Journal of the American College of Cardiology (JACC).
Flavanols are phytonutrient compounds that are found naturally in apples, grapes, tea, cocoa and cherries, which account for the antioxidant effect provided by red wine and green tea. The study found a protective effect from a cocoa drink with 375 mg of flavanols, but according to researchers, a standard or recommended dosage has not yet been defined to achieve optimal health benefit.
The UCSF team has shown for the first time that one of the possible mechanisms of flavanol's benefit is an increase in the circulation of so-called angiogenic cells in the blood. These cells, also known as early endothelial progenitor cells, are critical for the repair process after vascular injury, and perform function and maintenance roles in the endothelium. Endothelium is the thin layer of cells that line the interior wall of blood vessels.
"Reduced blood vessel function is a hallmark of early development of coronary artery disease," said cardiologist Yerem Yeghiazarians, MD, senior author, associate professor of medicine, and researcher in the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. "If we can improve the health and function of damaged blood vessels, heart disease patients will have a better chance of survival."
In 2005, researchers reported that an increased level of circulating angiogenic cells is associated with a decreased risk of death from cardiovascular causes (New England Journal of Medicine by Werner, N., et al.)
In the current study, the benefit seen from the two-fold increase in circulating angiogenic cells was similar to that achieved by therapy with statins and with lifestyle changes such as exercise and smoking cessation. The benefit demonstrated with cocoa flavanol therapy occurred in addition to the medical regimen already being taken by study participants.
"Our data support the concept that dietary flavanols at the levels provided - in tandem with current medical therapy - are safe, improve cardiovascular function, and increase circulating angiogenic cells, which have previously been shown to correlate positively with long-term cardiovascular outcomes" said Yeghiazarians. "Long-term trials examining the effects of high-flavanol diets on cardiovascular health and function are warranted, but these early findings help us understand how these compounds impact the function of damaged blood vessels."
The study included 16 coronary artery disease patients aged 64 years (±three years) who received a high-flavanol cocoa drink (containing 375 mg of flavanols) twice a day over 30 days and then a nutrient-matched low-flavanol cocoa drink (containing 9mg flavanols) twice a day over 30 days.
The study was randomized, controlled and "masked", meaning both the doctors and patients were prevented from knowing which variation of the cocoa drink a patient was drinking at a given time until after the study was completed. The patients continued taking all regular medications for their underlying heart disease during the study period, including statin medications for lowering the cholesterol levels to recommended goals.
Researchers calculated the outcome of the cocoa intervention using blood pressure readings, ultrasound to measure dilation of the brachial artery, and cell assays to calculate the number and behavior of circulating angiogenic cells. The tests showed a 47 percent improvement in vasodilation, or widening rather than constriction, of the brachial artery in the high-flavanol time period compared to the low-flavanol period. In addition, circulating angiogenic cells increased 2.2-fold and systolic blood pressure decreased among the high-flavanol versus low-flavanol periods.
"This is exciting data," Yeghiazarians added. "Our findings demonstrate that a further increase in endothelial function and improvement in blood pressure can be achieved by complementing standard treatment with a flavanol-rich diet. The 80 million Americans impacted by heart disease may be glad to hear this." Notably, the therapy did not influence fasting glucose levels of study participants. (Fasting glucose is the standard for measuring an individual's blood sugar level to diagnose conditions such as diabetes and heart disease).
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