Middle-aged men and women who engage in high levels of physical activity may be unknowingly causing damage to their knees and increasing their risk for osteoarthritis, according to a study presented today at the annual meeting of the Radiological Society of North America (RSNA).
"Our data suggest that people with higher physical activity levels may be at greater risk for developing knee abnormalities and, thus, at higher risk for developing osteoarthritis," said Christoph Stehling, M.D., research fellow in the Department of Radiology and Biomedical Imaging at the University of California, San Francisco (UCSF) and radiology resident in the Department of Clinical Radiology, University of Muenster, Germany.
Osteoarthritis is a degenerative joint disease that causes pain, swelling and stiffness. According to the Centers for Disease Control and Prevention, osteoarthritis is the most common form of arthritis and affects an estimated 27 million American adults.
The UCSF study involved 236 asymptomatic participants who had not reported previous knee pain and were enrolled in the National Institutes of Health Osteoarthritis Initiative. Study participants included 136 women and 100 men, age 45 to 55, within a healthy weight range. The participants were separated into low-, middle-, and high-activity groups based on their responses to the Physical Activity Scale for the Elderly (PASE) questionnaire. PASE is a standard test that scores an older individual's physical activity level, based on the type of activity and the time spent doing it. Several factors contribute to the final PASE score, but a person whose activity level is classified as high typically might engage in several hours of walking, sports or other types of exercise per week, as well as yard work and other household chores.
Subsequent MRI analysis by two musculoskeletal radiologists indicated a relationship between physical activity levels and frequency and severity of knee damage. Specific knee abnormalities identified included meniscal lesions, cartilage lesions, bone marrow edema and ligament lesions. Abnormalities were associated solely with activity levels and were not age or gender specific.
"The prevalence of the knee abnormalities increased with the level of physical activity," Dr. Stehling said. "In addition, cartilage defects diagnosed in active people were more severe."
The findings also indicated that some activities carry a greater risk of knee damage over time.
"This study and previous studies by our group suggest that high-impact, weight-bearing physical activity, such as running and jumping, may be worse for cartilage health," Dr. Stehling said. "Conversely, low-impact activities, such as swimming and cycling, may protect diseased cartilage and prevent healthy cartilage from developing disease."
Dr. Stehling noted that there is a need for prospective studies to evaluate the influence of low-impact versus high-impact physical activity on disease progression.
Monday, November 30, 2009
Long-term physical activity has an anti-aging effect
Intensive exercise prevented shortening of telomeres, a protective effect against aging of the cardiovascular system, according to research reported in Circulation: Journal of the American Heart Association.
Researchers measured the length of telomeres — the DNA that bookends the chromosomes and protects the ends from damage — in blood samples from two groups of professional athletes and two groups who were healthy nonsmokers, but not regular exercisers.
The telomere shortening mechanism limits cells to a fixed number of divisions and can be regarded as a “biological clock.” Gradual shortening of telomeres through cell divisions leads to aging on the cellular level and may limit lifetimes. When the telomeres become critically short the cell undergoes death. The 2009 Nobel Prize in Physiology or Medicine was awarded to researchers who discovered the nature of telomeres and how chromosomes are protected by telomeres and the enzyme telomerase.
“The most significant finding of this study is that physical exercise of the professional athletes leads to activation of the important enzyme telomerase and stabilizes the telomere,” said Ulrich Laufs, M.D., the study’s lead author and professor of clinical and experimental medicine in the department of internal medicine at Saarland University in Homburg, Germany.
“This is direct evidence of an anti-aging effect of physical exercise. Physical exercise could prevent the aging of the cardiovascular system, reflecting this molecular principle.”
Essentially, the longer telomere of athletes is an efficient telomere. The body’s cells are constantly growing and dividing and eventually dying off, a process controlled by the chromosomes within each cell. These chromosomal “end caps” — which have been likened to the tips of shoelaces, preventing them from fraying — become shorter with each cell division, and when they’re gone, the cell dies. Short telomeres limit the number of cell divisions, Laufs said. In addition, the animal studies of Laufs and colleagues show that the regulation of telomere stabilizing proteins by exercise exerts important cellular functions beyond the regulation of telomere length itself by protecting from cellular deterioration and programmed cell death.
In the clinical study, researchers analyzed 32 professional runners, average age 20, from the German National Team of Track and Field. Their average running distance was about 73 kilometers (km), a little over 45 miles, per week.
Researchers compared the young professional athletes with middle-aged athletes with a history of continuous endurance exercise since their youth. Their average age was 51 and their average distance was about 80 km, or almost 50 miles, per week.
The two groups were evaluated against untrained athletes who were healthy nonsmokers, but who did not exercise regularly. They were matched for age with the professional athletes.
The fitness level of the athletes was superior to the untrained individuals. The athletes had a slower resting heart rate, lower blood pressure and body mass index, and a more favorable cholesterol profile, researchers said.
Long-term exercise training activates telomerase and reduces telomere shortening in human leukocytes. The age-dependent telomere loss was lower in the master athletes who had performed endurance exercising for several decades.
“Our data improves the molecular understanding of the protective effects of exercise on the vessel wall and underlines the potency of physical training in reducing the impact of age-related disease,” Laufs said.
Researchers measured the length of telomeres — the DNA that bookends the chromosomes and protects the ends from damage — in blood samples from two groups of professional athletes and two groups who were healthy nonsmokers, but not regular exercisers.
The telomere shortening mechanism limits cells to a fixed number of divisions and can be regarded as a “biological clock.” Gradual shortening of telomeres through cell divisions leads to aging on the cellular level and may limit lifetimes. When the telomeres become critically short the cell undergoes death. The 2009 Nobel Prize in Physiology or Medicine was awarded to researchers who discovered the nature of telomeres and how chromosomes are protected by telomeres and the enzyme telomerase.
“The most significant finding of this study is that physical exercise of the professional athletes leads to activation of the important enzyme telomerase and stabilizes the telomere,” said Ulrich Laufs, M.D., the study’s lead author and professor of clinical and experimental medicine in the department of internal medicine at Saarland University in Homburg, Germany.
“This is direct evidence of an anti-aging effect of physical exercise. Physical exercise could prevent the aging of the cardiovascular system, reflecting this molecular principle.”
Essentially, the longer telomere of athletes is an efficient telomere. The body’s cells are constantly growing and dividing and eventually dying off, a process controlled by the chromosomes within each cell. These chromosomal “end caps” — which have been likened to the tips of shoelaces, preventing them from fraying — become shorter with each cell division, and when they’re gone, the cell dies. Short telomeres limit the number of cell divisions, Laufs said. In addition, the animal studies of Laufs and colleagues show that the regulation of telomere stabilizing proteins by exercise exerts important cellular functions beyond the regulation of telomere length itself by protecting from cellular deterioration and programmed cell death.
In the clinical study, researchers analyzed 32 professional runners, average age 20, from the German National Team of Track and Field. Their average running distance was about 73 kilometers (km), a little over 45 miles, per week.
Researchers compared the young professional athletes with middle-aged athletes with a history of continuous endurance exercise since their youth. Their average age was 51 and their average distance was about 80 km, or almost 50 miles, per week.
The two groups were evaluated against untrained athletes who were healthy nonsmokers, but who did not exercise regularly. They were matched for age with the professional athletes.
The fitness level of the athletes was superior to the untrained individuals. The athletes had a slower resting heart rate, lower blood pressure and body mass index, and a more favorable cholesterol profile, researchers said.
Long-term exercise training activates telomerase and reduces telomere shortening in human leukocytes. The age-dependent telomere loss was lower in the master athletes who had performed endurance exercising for several decades.
“Our data improves the molecular understanding of the protective effects of exercise on the vessel wall and underlines the potency of physical training in reducing the impact of age-related disease,” Laufs said.
CPR WORKS W/0 M-TO-M BUT NOT W/O OXYGEN
People can survive cardiac arrest if they receive only chest compressions during attempts to revive them – as advised by the current American Heart Association guidelines. But they cannot survive without access to oxygen sometime during the resuscitation effort, research suggests.
Scientists tested different scenarios in an animal study of cardiac arrest. Rats received either 100 percent oxygen, 21 percent oxygen – the equivalent of room air – or no oxygen (100 percent nitrogen) at the same time they received cardiopulmonary resuscitation (CPR).
About 80 percent of the rats survived regardless of the percentage of oxygen they received along with chest compressions. However, in the group receiving no oxygen, only one animal could be resuscitated.
Though these animals received the oxygen via ventilation, people who suffer cardiac arrest in a public setting would more likely obtain some oxygen by gasping during CPR or by receiving some air from a vacuum effect resulting from chest compressions, researchers say.
“The study showed that there is a need for oxygen. How much oxygen is needed remains unknown. There is probably a sweet spot in there somewhere,” said Mark Angelos, professor of emergency medicine at Ohio State University and senior author of the study.
“For the first few minutes, it’s probably right just to push on the chest. But at some point you probably need to add oxygen, however you can – maybe mouth-to-mouth or with supplemental oxygen. Where that sweet spot is is not yet clear.”
The research is published in a recent issue of the journal Resuscitation.
According to the American Heart Association, almost 80 percent of cardiac arrests that take place outside a hospital occur at home and are witnessed by a family member. Yet only 6.4 percent of sudden cardiac arrest victims survive because most witnesses do not know how to perform CPR.
The association is in the midst of a new campaign touting “hands-only” CPR, urging people to call 911 and push “hard and fast” in the center of the chest of a person in cardiac arrest.
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“In a public setting, presumably we don’t have any options. We see that ventilating with room air is just as good as supplemental oxygen,” he said. “However, we also know now that too little or the absence of any ventilation might be harmful, at least over time, due to the lack of oxygen.”
Angelos said his research is not intended to counter the current guidelines. Instead, scientists continue to study the intricacies of the resuscitation process in the pursuit of ways to improve the potential for survival after cardiac arrest.
Approximately 30 percent of cardiac arrest patients will survive long enough to be hospitalized. But far fewer are ever discharged from the hospital; most typically die of heart failure or brain damage resulting from an extended loss of oxygen to the brain, said Angelos, also an investigator in Ohio State’s Davis Heart and Lung Research Institute.
In the study, Angelos and colleagues imposed six minutes of cardiac arrest on 33 rats before CPR was started. During CPR, animals were ventilated with either 100 percent oxygen or 21 percent oxygen.
A control group of rats received nitrogen, which eliminated oxygen from their lungs. This scenario allowed for lab comparisons, but was not intended to mimic normal conditions because people would likely have some residual oxygen in their lungs and blood even during cardiac arrest.
CPR was continued until the surviving animals experienced what is called the “return of spontaneous circulation,” when the heart pumped blood on its own. All animals receiving oxygen returned to spontaneous circulation at approximately the same time, between about 90 seconds and two minutes after CPR began.
All surviving animals continued to receive the same levels of oxygen that they had received during CPR for two minutes after their hearts started working, and then they were all transferred to 100 percent oxygen for an hour.
“That’s pretty typical for a hospitalized cardiac arrest victim, to get a high concentration of oxygen early on,” Angelos said.
One rat unexpectedly survived CPR without any oxygen, but died within 72 hours. Among the rats receiving oxygen during CPR, nine of 11 (82 percent) of the rats in the 21-percent oxygen group survived CPR, and 10 of 12 (83 percent) of the rats receiving 100 percent oxygen survived. At the 72-hour mark, those figures had dropped: 77 percent of the room-air rats were still alive, and 80 percent of 100-percent oxygen rats were still living.
Neurological tests showed that five of seven (71 percent) of the room-air rats and three of eight (38 percent) of the rats on 100-percent oxygen during CPR returned to normal brain function at 72 hours. The researchers considered these findings secondary to the initial finding that oxygen was required for success during the initial resuscitation process, Angelos noted.
“In a public setting, presumably we don’t have any options. We see that ventilating with room air is just as good as supplemental oxygen,” he said. “However, we also know now that too little or the absence of any ventilation might be harmful, at least over time, due to the lack of oxygen.”
Generally, Angelos noted, the concern has been too much ventilation, which lessens the effectiveness of CPR.
Scientists tested different scenarios in an animal study of cardiac arrest. Rats received either 100 percent oxygen, 21 percent oxygen – the equivalent of room air – or no oxygen (100 percent nitrogen) at the same time they received cardiopulmonary resuscitation (CPR).
About 80 percent of the rats survived regardless of the percentage of oxygen they received along with chest compressions. However, in the group receiving no oxygen, only one animal could be resuscitated.
Though these animals received the oxygen via ventilation, people who suffer cardiac arrest in a public setting would more likely obtain some oxygen by gasping during CPR or by receiving some air from a vacuum effect resulting from chest compressions, researchers say.
“The study showed that there is a need for oxygen. How much oxygen is needed remains unknown. There is probably a sweet spot in there somewhere,” said Mark Angelos, professor of emergency medicine at Ohio State University and senior author of the study.
“For the first few minutes, it’s probably right just to push on the chest. But at some point you probably need to add oxygen, however you can – maybe mouth-to-mouth or with supplemental oxygen. Where that sweet spot is is not yet clear.”
The research is published in a recent issue of the journal Resuscitation.
According to the American Heart Association, almost 80 percent of cardiac arrests that take place outside a hospital occur at home and are witnessed by a family member. Yet only 6.4 percent of sudden cardiac arrest victims survive because most witnesses do not know how to perform CPR.
The association is in the midst of a new campaign touting “hands-only” CPR, urging people to call 911 and push “hard and fast” in the center of the chest of a person in cardiac arrest.
Email this to a friend
“In a public setting, presumably we don’t have any options. We see that ventilating with room air is just as good as supplemental oxygen,” he said. “However, we also know now that too little or the absence of any ventilation might be harmful, at least over time, due to the lack of oxygen.”
Angelos said his research is not intended to counter the current guidelines. Instead, scientists continue to study the intricacies of the resuscitation process in the pursuit of ways to improve the potential for survival after cardiac arrest.
Approximately 30 percent of cardiac arrest patients will survive long enough to be hospitalized. But far fewer are ever discharged from the hospital; most typically die of heart failure or brain damage resulting from an extended loss of oxygen to the brain, said Angelos, also an investigator in Ohio State’s Davis Heart and Lung Research Institute.
In the study, Angelos and colleagues imposed six minutes of cardiac arrest on 33 rats before CPR was started. During CPR, animals were ventilated with either 100 percent oxygen or 21 percent oxygen.
A control group of rats received nitrogen, which eliminated oxygen from their lungs. This scenario allowed for lab comparisons, but was not intended to mimic normal conditions because people would likely have some residual oxygen in their lungs and blood even during cardiac arrest.
CPR was continued until the surviving animals experienced what is called the “return of spontaneous circulation,” when the heart pumped blood on its own. All animals receiving oxygen returned to spontaneous circulation at approximately the same time, between about 90 seconds and two minutes after CPR began.
All surviving animals continued to receive the same levels of oxygen that they had received during CPR for two minutes after their hearts started working, and then they were all transferred to 100 percent oxygen for an hour.
“That’s pretty typical for a hospitalized cardiac arrest victim, to get a high concentration of oxygen early on,” Angelos said.
One rat unexpectedly survived CPR without any oxygen, but died within 72 hours. Among the rats receiving oxygen during CPR, nine of 11 (82 percent) of the rats in the 21-percent oxygen group survived CPR, and 10 of 12 (83 percent) of the rats receiving 100 percent oxygen survived. At the 72-hour mark, those figures had dropped: 77 percent of the room-air rats were still alive, and 80 percent of 100-percent oxygen rats were still living.
Neurological tests showed that five of seven (71 percent) of the room-air rats and three of eight (38 percent) of the rats on 100-percent oxygen during CPR returned to normal brain function at 72 hours. The researchers considered these findings secondary to the initial finding that oxygen was required for success during the initial resuscitation process, Angelos noted.
“In a public setting, presumably we don’t have any options. We see that ventilating with room air is just as good as supplemental oxygen,” he said. “However, we also know now that too little or the absence of any ventilation might be harmful, at least over time, due to the lack of oxygen.”
Generally, Angelos noted, the concern has been too much ventilation, which lessens the effectiveness of CPR.
Wednesday, November 25, 2009
High salt = strokes and cardiovascular disease
Eating high amounts of salt is linked to a significantly higher risk of strokes and cardiovascular disease, states a paper published today in the British Medical Journal.
The research was carried out jointly by the World Health Organization's Collaborating Centre for Nutrition, based at the University of Warwick and University Hospital in Coventry, UK, and the European Society of Hypertension Excellence Centre in Hypertension based at the Department of Clinical and Experimental Medicine, Federico II University Medical School in Naples, Italy.
The study looked at the relationship between the level of habitual dietary salt intake and the occurrence of stroke and cardiovascular disease by reviewing 13 prospective studies from the UK, Japan, USA, The Netherlands, Finland and China, including more than 170,000 participants, followed up for 3.5 to 19 years, who experienced nearly 11,000 vascular events.
The study provides unequivocal evidence of the direct link between high dietary salt intake and increased risk of stroke and cardiovascular disease. A 5 g lower daily salt intake would reduce stroke by 23% and total cardiovascular disease by 17%, thus averting 1.25 million fatal and non-fatal strokes, and almost 3 million vascular events worldwide each year. The effect is greater, the larger the difference in salt intake and increases with time.
Professor Francesco Cappuccio, Head of the World Health Organisation Collaboration Centre at Warwick Medical School said: "We have seen reductions in the salt content of several food items, due to the collaboration between governments, public health bodies and sectors of the industry on a voluntary basis. However, the progress towards the recommended targets has been slow. For population salt intake to approach the WHO targets within a reasonable time, a regulatory approach is necessary, in addition to health promotion campaigns, to reduce the burden of avoidable death, disability and associated costs to individuals and society caused by unacceptable high levels of salt in our diet".
"Habitual salt intake in most adult populations around the world exceeds 10 g per day", says Professor Pasquale Strazzullo, one of the senior authors, "and the World Health Organization recommends that daily intake should not exceed 5 grams. Our study supports current recommendations to reduce substantially salt intake worldwide to avoid unnecessary strokes and other cardiovascular events".
Cardiovascular disease is the first cause of death and disability in the world among people aged over 60 years and the second one among those 15 to 59 years old.
According to the World Health Organization, 62% of all strokes and 49% of coronary heart disease events are attributable to high blood pressure.
There is a direct causal relationship between levels of dietary salt intake and levels of blood pressure.
Most of the salt we eat comes from that added to food in the manufacturing process by industry, caterers and food producers.
The research was carried out jointly by the World Health Organization's Collaborating Centre for Nutrition, based at the University of Warwick and University Hospital in Coventry, UK, and the European Society of Hypertension Excellence Centre in Hypertension based at the Department of Clinical and Experimental Medicine, Federico II University Medical School in Naples, Italy.
The study looked at the relationship between the level of habitual dietary salt intake and the occurrence of stroke and cardiovascular disease by reviewing 13 prospective studies from the UK, Japan, USA, The Netherlands, Finland and China, including more than 170,000 participants, followed up for 3.5 to 19 years, who experienced nearly 11,000 vascular events.
The study provides unequivocal evidence of the direct link between high dietary salt intake and increased risk of stroke and cardiovascular disease. A 5 g lower daily salt intake would reduce stroke by 23% and total cardiovascular disease by 17%, thus averting 1.25 million fatal and non-fatal strokes, and almost 3 million vascular events worldwide each year. The effect is greater, the larger the difference in salt intake and increases with time.
Professor Francesco Cappuccio, Head of the World Health Organisation Collaboration Centre at Warwick Medical School said: "We have seen reductions in the salt content of several food items, due to the collaboration between governments, public health bodies and sectors of the industry on a voluntary basis. However, the progress towards the recommended targets has been slow. For population salt intake to approach the WHO targets within a reasonable time, a regulatory approach is necessary, in addition to health promotion campaigns, to reduce the burden of avoidable death, disability and associated costs to individuals and society caused by unacceptable high levels of salt in our diet".
"Habitual salt intake in most adult populations around the world exceeds 10 g per day", says Professor Pasquale Strazzullo, one of the senior authors, "and the World Health Organization recommends that daily intake should not exceed 5 grams. Our study supports current recommendations to reduce substantially salt intake worldwide to avoid unnecessary strokes and other cardiovascular events".
Cardiovascular disease is the first cause of death and disability in the world among people aged over 60 years and the second one among those 15 to 59 years old.
According to the World Health Organization, 62% of all strokes and 49% of coronary heart disease events are attributable to high blood pressure.
There is a direct causal relationship between levels of dietary salt intake and levels of blood pressure.
Most of the salt we eat comes from that added to food in the manufacturing process by industry, caterers and food producers.
Tuesday, November 24, 2009
Soy component may be key to fighting colon cancer
A study conducted by Children's Hospital & Research Center Oakland scientists identifies a new class of therapeutic agents found naturally in soy that can prevent and possibly treat colon cancer, the third most deadly form of cancer. Sphingadienes (SDs) are natural lipid molecules found in soy that research shows may be the key to fighting colon cancer.
The study, led by Julie Saba, MD, PhD, senior scientist and director of the Cancer Center at Children's Hospital Oakland Research Institute (CHORI), will be featured in the December 15, 2009 issue of Cancer Research. Soy has long been touted as protective against colon cancer, but Dr. Saba's team made the groundbreaking discovery that SDs naturally found in soy may underlie the benefits of soy products.
Dr. Saba and her team first identified SDs in the fruit fly, an organism that is sometimes used to study the genetics of human diseases. Further investigation indicated that elevated SDs actually induced the death of mutant cells in the fly, revealing SDs to be cytotoxic compounds (toxic to cells). Preventative colon cancer strategies often focus on cell death—a normal process the body uses to remove unhealthy or mutant cells, like cancer cells. Coupling this discovery with the finding that soy is a rich source of SDs, researchers made an innovative connection.
"It's very exciting," said Dr. Saba. "First, we are encouraged to find a natural molecule that could be consumed through soy products as a strategy to help prevent colon cancer. Second, this information is important because we can build on our understanding of the structure and metabolism of SDs in terms of developing new drugs to treat people who already have colon cancer. Uncovering how SDs exert their effects also helps us to find the most likely combinations of drugs that may work synergistically to eliminate cancer cells and mutant cells that could give rise to cancer."
Future research is needed to identify the best way to deliver SDs and to confirm the overall toxicity when the compounds are used for extended time periods and in combination with other agents. Dr. Saba, who has already received two grants to continue her research, also hopes to determine if SDs are effective in protection against other cancers.
Dr. Saba also acknowledges that future research is needed to determine if there are other components of soy that are beneficial in fighting colon cancer. In the meantime, Dr. Saba says, "I would be comfortable recommending soy products as a change in the diet that could protect against cancer. The more that soy is studied, the more of these protective agents are found, so it's a very healthy diet choice."
The study, led by Julie Saba, MD, PhD, senior scientist and director of the Cancer Center at Children's Hospital Oakland Research Institute (CHORI), will be featured in the December 15, 2009 issue of Cancer Research. Soy has long been touted as protective against colon cancer, but Dr. Saba's team made the groundbreaking discovery that SDs naturally found in soy may underlie the benefits of soy products.
Dr. Saba and her team first identified SDs in the fruit fly, an organism that is sometimes used to study the genetics of human diseases. Further investigation indicated that elevated SDs actually induced the death of mutant cells in the fly, revealing SDs to be cytotoxic compounds (toxic to cells). Preventative colon cancer strategies often focus on cell death—a normal process the body uses to remove unhealthy or mutant cells, like cancer cells. Coupling this discovery with the finding that soy is a rich source of SDs, researchers made an innovative connection.
"It's very exciting," said Dr. Saba. "First, we are encouraged to find a natural molecule that could be consumed through soy products as a strategy to help prevent colon cancer. Second, this information is important because we can build on our understanding of the structure and metabolism of SDs in terms of developing new drugs to treat people who already have colon cancer. Uncovering how SDs exert their effects also helps us to find the most likely combinations of drugs that may work synergistically to eliminate cancer cells and mutant cells that could give rise to cancer."
Future research is needed to identify the best way to deliver SDs and to confirm the overall toxicity when the compounds are used for extended time periods and in combination with other agents. Dr. Saba, who has already received two grants to continue her research, also hopes to determine if SDs are effective in protection against other cancers.
Dr. Saba also acknowledges that future research is needed to determine if there are other components of soy that are beneficial in fighting colon cancer. In the meantime, Dr. Saba says, "I would be comfortable recommending soy products as a change in the diet that could protect against cancer. The more that soy is studied, the more of these protective agents are found, so it's a very healthy diet choice."
Monday, November 23, 2009
Exercise Fights Strokes
Moderate-to-heavy exercise may reduce risk of stroke for men
Men who regularly take part in moderate-to-heavy intensity exercise such as jogging, tennis or swimming may be less likely to have a stroke than people who get no exercise or only light exercise, such as walking, golfing, or bowling, according to a study published in the November 24, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.
However, exercise did not have a protective effect against stroke for women. Women who took part in moderate-to-heavy intensity exercise did not have a reduced risk of stroke.
The study involved 3,298 people living in northern Manhattan, NY, with an average age of 69 who were followed for about nine years. During that time, there were 238 strokes. A total of 41 percent of the participants reported that they participated in no physical activity. Twenty percent regularly participated in moderate-to-heavy intensity activities.
Men who participated in moderate-to-heavy intensity activities were 63 percent less likely to have a stroke than people with no physical activity. The baseline risk of ischemic stroke over five years in the entire group was 4.3 percent; among those with moderate-to-heavy intensity activities the risk was 2.7 percent, and among those with no activity it was 4.6 percent.
"Taking part in moderate-to-heavy intensity physical activity may be an important factor in preventing stroke," said study author Joshua Z. Willey, MD, of Columbia University Medical Center and New York Presbyterian Hospital at Columbia. Willey is also a member of the American Academy of Neurology. "A large percentage of the participants were not taking part in any physical activities. This may be true of many elderly people who live in cities. Identifying ways to improve physical activity among these people may be a key goal for public health."
These results are contrary to some other studies that found that even light intensity physical activity reduced the risk of stroke. Willey said the number of participants may not have been large enough to detect subtle differences in the group that took part in only light physical activity.
Stroke is the leading cause of disability and the third-leading cause of death in the United States.
Men who regularly take part in moderate-to-heavy intensity exercise such as jogging, tennis or swimming may be less likely to have a stroke than people who get no exercise or only light exercise, such as walking, golfing, or bowling, according to a study published in the November 24, 2009, print issue of Neurology®, the medical journal of the American Academy of Neurology.
However, exercise did not have a protective effect against stroke for women. Women who took part in moderate-to-heavy intensity exercise did not have a reduced risk of stroke.
The study involved 3,298 people living in northern Manhattan, NY, with an average age of 69 who were followed for about nine years. During that time, there were 238 strokes. A total of 41 percent of the participants reported that they participated in no physical activity. Twenty percent regularly participated in moderate-to-heavy intensity activities.
Men who participated in moderate-to-heavy intensity activities were 63 percent less likely to have a stroke than people with no physical activity. The baseline risk of ischemic stroke over five years in the entire group was 4.3 percent; among those with moderate-to-heavy intensity activities the risk was 2.7 percent, and among those with no activity it was 4.6 percent.
"Taking part in moderate-to-heavy intensity physical activity may be an important factor in preventing stroke," said study author Joshua Z. Willey, MD, of Columbia University Medical Center and New York Presbyterian Hospital at Columbia. Willey is also a member of the American Academy of Neurology. "A large percentage of the participants were not taking part in any physical activities. This may be true of many elderly people who live in cities. Identifying ways to improve physical activity among these people may be a key goal for public health."
These results are contrary to some other studies that found that even light intensity physical activity reduced the risk of stroke. Willey said the number of participants may not have been large enough to detect subtle differences in the group that took part in only light physical activity.
Stroke is the leading cause of disability and the third-leading cause of death in the United States.
Flaxseed oil and osteoporosis
Animal studies suggest that adding flaxseed oil to the diet could reduce the risk of osteoporosis in post-menopausal women and women with diabetes, according to a report to be published in the International Journal of Food Safety, Nutrition and Public Health.
Mer Harvi and colleagues at the National Research Center, in Cairo, Egypt, have studied the effect of diabetes on bone health and evaluated how flaxseed oil in the diet might delay the onset of osteoporosis. The researchers studied 70 female albino rats of which 30 had their ovaries removed (ovx) to simulate the post-menopausal state and experimental diabetes was present in one group of rodents.
The researchers then classified the rats as control, sham, diabetic, diabetic received flaxseed oil in the diet, ovx, ovx-diabetic and ovx-diabetic received flaxseed oil in the diet.
After two months, the team collected urine and blood samples from the rats and measured serum insulin-like growth factor 1 (IGF-1) and the bone-creating protein osteocalcin. They found that these two compounds were present at higher levels in the ovx and the diabetic ovx groups, but much lower in the non-ovx diabetic group. The concentrations of IGF-1 and osteocalcin could be raised to normal levels by adding flaxseed oil to the diet.
The team also found that the levels of deoxypyridinoline in the urine were raised in the diabetic group. Deoxypyridinoline is normally present in healthy bone and its presence in urine is a specific marker for bone resorption associated with osteoporosis. Levels of this marker compound fell when the rats were given flaxseed oil.
The team concludes that diabetes has a more pronounced effect on bone health than ovariectomy and so may suggest that diabetes in post-menopausal women may also be a greater risk factor for osteoporosis than the decline in sex hormones associated with the menopause. However, their results suggest that flaxseed oil has a beneficial effect on bone mineral density and reduces markers associated with osteoporosis, suggesting that this dietary supplement could be beneficial to women with diabetes in reducing their risk of osteoporosis.
The team explains that the presence of so-called "n-3 fatty acids" in flaxseed oil may play a role in protecting the processes of matrix formation and bone mineralization, which are apparently compromised by diabetes and the menopause. "We recommend further investigations using animals and humans to confirm the effect of using dietary flaxseed oil to improve bone health and to prevent osteoporosis," Harvi and colleagues conclude.
Mer Harvi and colleagues at the National Research Center, in Cairo, Egypt, have studied the effect of diabetes on bone health and evaluated how flaxseed oil in the diet might delay the onset of osteoporosis. The researchers studied 70 female albino rats of which 30 had their ovaries removed (ovx) to simulate the post-menopausal state and experimental diabetes was present in one group of rodents.
The researchers then classified the rats as control, sham, diabetic, diabetic received flaxseed oil in the diet, ovx, ovx-diabetic and ovx-diabetic received flaxseed oil in the diet.
After two months, the team collected urine and blood samples from the rats and measured serum insulin-like growth factor 1 (IGF-1) and the bone-creating protein osteocalcin. They found that these two compounds were present at higher levels in the ovx and the diabetic ovx groups, but much lower in the non-ovx diabetic group. The concentrations of IGF-1 and osteocalcin could be raised to normal levels by adding flaxseed oil to the diet.
The team also found that the levels of deoxypyridinoline in the urine were raised in the diabetic group. Deoxypyridinoline is normally present in healthy bone and its presence in urine is a specific marker for bone resorption associated with osteoporosis. Levels of this marker compound fell when the rats were given flaxseed oil.
The team concludes that diabetes has a more pronounced effect on bone health than ovariectomy and so may suggest that diabetes in post-menopausal women may also be a greater risk factor for osteoporosis than the decline in sex hormones associated with the menopause. However, their results suggest that flaxseed oil has a beneficial effect on bone mineral density and reduces markers associated with osteoporosis, suggesting that this dietary supplement could be beneficial to women with diabetes in reducing their risk of osteoporosis.
The team explains that the presence of so-called "n-3 fatty acids" in flaxseed oil may play a role in protecting the processes of matrix formation and bone mineralization, which are apparently compromised by diabetes and the menopause. "We recommend further investigations using animals and humans to confirm the effect of using dietary flaxseed oil to improve bone health and to prevent osteoporosis," Harvi and colleagues conclude.
Vitamin D Summary
A string of recent discoveries about the multiple health benefits of vitamin D has renewed interest in this multi-purpose nutrient, increased awareness of the huge numbers of people who are deficient in it, spurred research and even led to an appreciation of it as "nature's antibiotic."
On issues ranging from the health of your immune system to prevention of heart disease and even vulnerability to influenza, vitamin D is now seen as one of the most critical nutrients for overall health. But it's also one of those most likely to be deficient – especially during winter when production of the "sunshine vitamin" almost grinds to a halt for millions of people in the United States, Europe and other northern temperate zones.
Analogs of the vitamin are even being considered for use as new therapies against tuberculosis, AIDS, and other concerns. And federal experts are considering an increase in the recommended daily intake of the vitamin as more evidence of its value emerges, especially for the elderly.
"About 70 percent of the population of the United States has insufficient levels of vitamin D," said Adrian Gombart, a principal investigator with the Linus Pauling Institute at Oregon State University. "This is a critical issue as we learn more about the many roles it may play in fighting infection, balancing your immune response, helping to address autoimmune problems, and even preventing heart disease."
Those issues were just outlined in a new publication in Future Microbiology, a professional journal, on the latest findings on vitamin D research, at OSU and in many other programs around the world.
Of particular interest are findings made recently by OSU scientists that vitamin D induces the "expression" of cathelicidin, an antimicrobial peptide gene. This explains in part how it helps serve as the first line of defense in your immune response against minor wounds, cuts, and both bacterial and viral infections. Experts believe advances in the use of cathelicidin may form the basis for new therapies.
Once believed to be related primarily to bone health and rickets – a disease caused by chronic deficiency of vitamin D – it's now understood that optimal levels of this nutrient influence much more than that.
"Vitamin D insufficiency and deficiency is a world-wide, public health problem in both developed and developing nations," the new report concluded. "Nearly one billion people world-wide are deficient."
Vitamin D can be obtained from the diet, often through supplemented foods such as milk, but those sources are rarely adequate, experts say. Most people get the bulk of this fat-soluble vitamin from the UV-B radiation in sun exposure, which naturally causes the skin to produce it. However, people with dark skin, infants and almost anyone living north of about 40 degrees latitude – which is a huge portion of the U.S. population and most of Europe– are often deficient after months of inadequate winter sunshine.
Among the values and observations about vitamin D that are outlined in the new report:
• Low levels of circulating vitamin D are associated with increased risk and mortality from cancer.
• Vitamin D plays an important role in activating the immune system, fostering the "innate" immune response and controlling over-reaction of adaptive immunity, and as such may help control autoimmune diseases such as multiple sclerosis, psoriasis and rheumatoid arthritis.
• Cathelicidin can profoundly boost the innate immune system, and could form the basis for new therapies to combat pathogenic infections.
• The regulation of cathelicidin by vitamin D, a unique biological pathway for the function of vitamin D that could help explain its multiple roles in proper immune function, is so important that it's only known to exist in two groups of animals - humans and non-human primates - and has been conserved in them through millions of years of evolution.
• Vitamin D deficiency is a risk factor for tuberculosis, was historically used to treat it, and analogs of it may provide the basis for new therapeutic approaches not only to that disease but also HIV infection.
• Epidemiological studies show a link between vitamin D deficiency and increased rates of respiratory infection and influenza, and it has been hypothesized that flu epidemics may be the result of vitamin D deficiency.
• Higher levels of a protein linked to vitamin D have been associated with reduced infections and longer survival of dialysis patients.
• Vitamin D has important roles in reducing inflammation, blood pressure and helping to protect against heart disease.
There is still much to explore about the mechanisms of action of vitamin D, the potential use of synthetic analogs of it in new therapies, and its role in fighting infection, Gombart said. Since only primates and humans have the same biological pathways for use of vitamin D to regulate cathelicidin, studies have been constrained by the lack of appropriate animal models for research, he said. OSU scientists hope to address that by creation of a line of genetically modified mice that have some of these characteristics.
One compelling new study just done by researchers at the Intermountain Medical Center in Utah, and presented at a meeting of the American Heart Association, followed for more than a year nearly 28,000 patients ages 50 or older with no prior history of cardiovascular disease. It found that in patients with very low levels of vitamin D – compared to those with normal levels – 77 percent were more likely to die, 45 percent were more likely to develop coronary artery disease, and 78 percent were more likely to have a stroke.
On issues ranging from the health of your immune system to prevention of heart disease and even vulnerability to influenza, vitamin D is now seen as one of the most critical nutrients for overall health. But it's also one of those most likely to be deficient – especially during winter when production of the "sunshine vitamin" almost grinds to a halt for millions of people in the United States, Europe and other northern temperate zones.
Analogs of the vitamin are even being considered for use as new therapies against tuberculosis, AIDS, and other concerns. And federal experts are considering an increase in the recommended daily intake of the vitamin as more evidence of its value emerges, especially for the elderly.
"About 70 percent of the population of the United States has insufficient levels of vitamin D," said Adrian Gombart, a principal investigator with the Linus Pauling Institute at Oregon State University. "This is a critical issue as we learn more about the many roles it may play in fighting infection, balancing your immune response, helping to address autoimmune problems, and even preventing heart disease."
Those issues were just outlined in a new publication in Future Microbiology, a professional journal, on the latest findings on vitamin D research, at OSU and in many other programs around the world.
Of particular interest are findings made recently by OSU scientists that vitamin D induces the "expression" of cathelicidin, an antimicrobial peptide gene. This explains in part how it helps serve as the first line of defense in your immune response against minor wounds, cuts, and both bacterial and viral infections. Experts believe advances in the use of cathelicidin may form the basis for new therapies.
Once believed to be related primarily to bone health and rickets – a disease caused by chronic deficiency of vitamin D – it's now understood that optimal levels of this nutrient influence much more than that.
"Vitamin D insufficiency and deficiency is a world-wide, public health problem in both developed and developing nations," the new report concluded. "Nearly one billion people world-wide are deficient."
Vitamin D can be obtained from the diet, often through supplemented foods such as milk, but those sources are rarely adequate, experts say. Most people get the bulk of this fat-soluble vitamin from the UV-B radiation in sun exposure, which naturally causes the skin to produce it. However, people with dark skin, infants and almost anyone living north of about 40 degrees latitude – which is a huge portion of the U.S. population and most of Europe– are often deficient after months of inadequate winter sunshine.
Among the values and observations about vitamin D that are outlined in the new report:
• Low levels of circulating vitamin D are associated with increased risk and mortality from cancer.
• Vitamin D plays an important role in activating the immune system, fostering the "innate" immune response and controlling over-reaction of adaptive immunity, and as such may help control autoimmune diseases such as multiple sclerosis, psoriasis and rheumatoid arthritis.
• Cathelicidin can profoundly boost the innate immune system, and could form the basis for new therapies to combat pathogenic infections.
• The regulation of cathelicidin by vitamin D, a unique biological pathway for the function of vitamin D that could help explain its multiple roles in proper immune function, is so important that it's only known to exist in two groups of animals - humans and non-human primates - and has been conserved in them through millions of years of evolution.
• Vitamin D deficiency is a risk factor for tuberculosis, was historically used to treat it, and analogs of it may provide the basis for new therapeutic approaches not only to that disease but also HIV infection.
• Epidemiological studies show a link between vitamin D deficiency and increased rates of respiratory infection and influenza, and it has been hypothesized that flu epidemics may be the result of vitamin D deficiency.
• Higher levels of a protein linked to vitamin D have been associated with reduced infections and longer survival of dialysis patients.
• Vitamin D has important roles in reducing inflammation, blood pressure and helping to protect against heart disease.
There is still much to explore about the mechanisms of action of vitamin D, the potential use of synthetic analogs of it in new therapies, and its role in fighting infection, Gombart said. Since only primates and humans have the same biological pathways for use of vitamin D to regulate cathelicidin, studies have been constrained by the lack of appropriate animal models for research, he said. OSU scientists hope to address that by creation of a line of genetically modified mice that have some of these characteristics.
One compelling new study just done by researchers at the Intermountain Medical Center in Utah, and presented at a meeting of the American Heart Association, followed for more than a year nearly 28,000 patients ages 50 or older with no prior history of cardiovascular disease. It found that in patients with very low levels of vitamin D – compared to those with normal levels – 77 percent were more likely to die, 45 percent were more likely to develop coronary artery disease, and 78 percent were more likely to have a stroke.
Thursday, November 19, 2009
Beneficial Effects of Aspirin in Cardiovascular Disease
On November 15, 2009, Florida Atlantic University (FAU) researcher Charles H. Hennekens, M.D., the first Sir Richard Doll Research Professor in the Charles E. Schmidt College of Biomedical Science will present at the American Heart Association's Annual Scientific Sessions meeting in Orlando, FL, the first data in humans to show that all doses of aspirin used in clinical practice increase nitric oxide. Nitric oxide is released from the blood vessel wall and may decrease the development and progression of plaques leading to heart attacks and strokes.
Hennekens was the first to demonstrate that aspirin can prevent a first heart attack or a first stroke.
The abstract, titled "Usual Doses of Aspirin Increase Nitric Acid Formation in Humans" is published in the November 2009 issue of Circulation, the official journal of the American Heart Association.
FAU researchers conducted a randomized trial in patients at high risk of a first heart attack or stroke and assigned them to different doses of aspirin for 12 weeks. All doses produced highly significant beneficial effects on two important and well documented markers of nitric oxide formation.
"While the ability of aspirin to decrease the clumping of blood platelets is sufficient to explain why the drug decreases heart attacks and strokes, these data suggest a new and novel mechanism," said Hennekens.
Co-author and project director of the trial and affiliate clinical instructor of clinical science and medical education, Wendy Schneider, MSN, RN, said, "We are proposing new and longer term research to test whether this hypothesis has clinical or public health relevance."
The American Heart Association recommends aspirin use for patients who've had a myocardial infarction (heart attack), unstable angina, ischemic stroke (caused by blood clot) or transient ischemic attacks (TIAs or "little strokes"), if not contraindicated. This recommendation is based on sound evidence from clinical trials showing that aspirin helps prevent the recurrence of such events as heart attack, hospitalization for recurrent angina, second strokes, etc. (secondary prevention). Studies show aspirin also helps prevent these events from occurring in people at high risk (primary prevention).
Hennekens was the first to demonstrate that aspirin can prevent a first heart attack or a first stroke.
The abstract, titled "Usual Doses of Aspirin Increase Nitric Acid Formation in Humans" is published in the November 2009 issue of Circulation, the official journal of the American Heart Association.
FAU researchers conducted a randomized trial in patients at high risk of a first heart attack or stroke and assigned them to different doses of aspirin for 12 weeks. All doses produced highly significant beneficial effects on two important and well documented markers of nitric oxide formation.
"While the ability of aspirin to decrease the clumping of blood platelets is sufficient to explain why the drug decreases heart attacks and strokes, these data suggest a new and novel mechanism," said Hennekens.
Co-author and project director of the trial and affiliate clinical instructor of clinical science and medical education, Wendy Schneider, MSN, RN, said, "We are proposing new and longer term research to test whether this hypothesis has clinical or public health relevance."
The American Heart Association recommends aspirin use for patients who've had a myocardial infarction (heart attack), unstable angina, ischemic stroke (caused by blood clot) or transient ischemic attacks (TIAs or "little strokes"), if not contraindicated. This recommendation is based on sound evidence from clinical trials showing that aspirin helps prevent the recurrence of such events as heart attack, hospitalization for recurrent angina, second strokes, etc. (secondary prevention). Studies show aspirin also helps prevent these events from occurring in people at high risk (primary prevention).
Wednesday, November 18, 2009
Green tea may protect liver cells
Green tea may protect liver cells and reduce the deposition of collagen fibers in the liver. Green tea provides a safe and effective strategy for improving hepatic fibrosis.
Several studies have shown that lipid peroxidation stimulates collagen production in fibroblasts and hepatic stellate cells (HSC), and plays an important role in the development of liver fibrosis. Hepatoprotective effects of green tea against carbon tetrachloride, cholestasis and alcohol induced liver fibrosis were reported in many studies. However, the hepatoprotective effect of green tea in dimethylnitrosamine (DMN)-induced models has not been studied.
A research article published on November 7, 2009 in the World Journal of Gastroenterology addresses this question. The research team, led by Prof. Hong-Yon Cho from Korea University examined the protective effect of green tea extract (GT) on hepatic fibrosis in a rat HSC line and in a rat model of DMN-induced hepatic fibrosis.
The results showed GT administration prevented the development of hepatic fibrosis in the rat model of DMN-induced liver fibrosis. These results were confirmed both by liver histology and by quantitative measurement of hepatic hydroxyproline content, a marker of liver collagen deposition. Accordingly, inhibition of proliferation, reduced collagen deposition, and type 1 collagen expression were observed in activated HSC-T6 cells following GT treatment. These results imply that GT reduced the proliferation of activated HSC and down regulated the collagen content and expression of collagen type 1, thereby ameliorating hepatic fibrosis.
The researchers drew a conclusion that
Several studies have shown that lipid peroxidation stimulates collagen production in fibroblasts and hepatic stellate cells (HSC), and plays an important role in the development of liver fibrosis. Hepatoprotective effects of green tea against carbon tetrachloride, cholestasis and alcohol induced liver fibrosis were reported in many studies. However, the hepatoprotective effect of green tea in dimethylnitrosamine (DMN)-induced models has not been studied.
A research article published on November 7, 2009 in the World Journal of Gastroenterology addresses this question. The research team, led by Prof. Hong-Yon Cho from Korea University examined the protective effect of green tea extract (GT) on hepatic fibrosis in a rat HSC line and in a rat model of DMN-induced hepatic fibrosis.
The results showed GT administration prevented the development of hepatic fibrosis in the rat model of DMN-induced liver fibrosis. These results were confirmed both by liver histology and by quantitative measurement of hepatic hydroxyproline content, a marker of liver collagen deposition. Accordingly, inhibition of proliferation, reduced collagen deposition, and type 1 collagen expression were observed in activated HSC-T6 cells following GT treatment. These results imply that GT reduced the proliferation of activated HSC and down regulated the collagen content and expression of collagen type 1, thereby ameliorating hepatic fibrosis.
The researchers drew a conclusion that
Tuesday, November 17, 2009
How fish is cooked affects heart-health benefits of omega-3 fatty acids
If you eat fish to gain the heart-health benefits of its omega-3 fatty acids, baked or boiled fish is better than fried, salted or dried, according to research presented at the American Heart Association’s Scientific Sessions 2009.
And, researchers said, adding low-sodium soy sauce or tofu will enhance the benefits.
“It appears that boiling or baking fish with low-sodium soy sauce (shoyu) and tofu is beneficial, while eating fried, salted or dried fish is not,” said Lixin Meng, M.S., lead researcher of the study and Ph.D. candidate at the University of Hawaii at Manoa. “In fact, these methods of preparation may contribute to your risk. We did not directly compare boiled or baked fish vs. fried fish, but one can tell from the (risk) ratios, boiled or baked fish is in the protective direction but not fried fish.”
The findings also suggest that the cardioprotective benefits vary by gender and ethnicity — perhaps because of the preparation methods, genetic susceptibility or hormonal factors.
Many studies have suggested that eating omega-3 fatty acids reduces the risk of heart disease; however, little is known about which source is most beneficial.
In this study, researchers examined the source, type, amount and frequency of dietary omega-3 ingestion among gender and ethnic groups. Participants were part of the Multiethnic Cohort living in Hawaii and Los Angeles County when they were recruited between 1993 and 1996. The group consisted of 82,243 men and 103,884 women of African-American, Caucasian, Japanese, Native Hawaiian and Latino descent ages 45 to 75 years old with no history of heart disease.
Researchers divided their intake of canned tuna, other canned fish, fish excluding shell fish, or soy products that contain plant omega-3s (soy, tofu and shoyu) into quintiles, quartiles, or tertiles when applicable. They also surveyed the preparation methods: raw, baked, boiled; fried; salted or dried. The initial study did not consider grilled fish.
Those in the highest quintile consumed a median 3.3 grams of omega-3 fatty acids a day. The lowest quintile consumed a median of 0.8 grams a day.
Omega-3 intake was inversely associated with overall risk of death due to heart disease in men — a trend mainly observed in Caucasians, Japanese Americans and Latinos. However, there weren’t many blacks or Hawaiians in the study, so the results should be interpreted cautiously, Meng said.
Overall, men who ate about 3.3 grams per day of omega-3 fatty acids had a 23 percent lower risk of cardiac death compared to those who ate 0.8 grams daily.
“Clearly, we are seeing that the higher the dietary omega-3 intake, the lower the risk of dying from heart disease among men,” Meng said.
Japanese and Hawaiians eat fish more often compared to whites, blacks and Latinos, and they prepare fish in a variety of methods, Meng noted.
For women, the omega-3 effect was cardioprotective at each level of consumption but not consistently significant, Meng said. Salted and dried fish was a risk factor in women.
In contrast, adding less than 1.1 gram/day shoyu and teriyaki sauce at the dinner table was protective for men but not for greater than 1.1 gram/day. For women, shoyu use showed a clear inverse relationship to death from heart disease. She noted that shoyu that is high in sodium can raise blood pressure, so she stressed low-sodium products. Eating tofu also had a cardioprotective effect in all ethnic groups.
“My guess is that, for women, eating omega-3s from shoyu and tofu that contain other active ingredients such as phytoestrogens, might have a stronger cardioprotective effect than eating just omega-3s,” said Meng, noting that further studies are needed to confirm the hypothesis.
During the average 11.9 years of follow-up, 4,516 heart-related deaths occurred in the group, according to state and national death records, which were cross-referenced through the end of 2005.
The study didn’t consider possible dietary changes over time; subjects who were diagnosed with heart disease after their baseline food intake surveys might have modified their eating habits. Further, the study didn’t account for the possible effects of fish-oil supplementation.
In light of these limitations, the researchers plan to include subjects’ dietary patterns over time and a cross-validation of their omega-3 levels through blood analysis.
“Our findings can help educate people on how much fish to eat and how to cook it to prevent heart disease,” Meng said. “Alternately, if it is verified that the interactions between fish consumption, risk factors and ethnicity are due to genetic susceptibility, the heart-disease prevention message can be personalized to ethnic groups, and future study could identify susceptibility at the genetic level.”
The American Heart Association recommends eating fish (particularly fatty fish) at least two times a week and eating tofu and other forms of soybeans, canola, walnut and flaxseed, and their oils. Learn specific information on the recommendations.
And, researchers said, adding low-sodium soy sauce or tofu will enhance the benefits.
“It appears that boiling or baking fish with low-sodium soy sauce (shoyu) and tofu is beneficial, while eating fried, salted or dried fish is not,” said Lixin Meng, M.S., lead researcher of the study and Ph.D. candidate at the University of Hawaii at Manoa. “In fact, these methods of preparation may contribute to your risk. We did not directly compare boiled or baked fish vs. fried fish, but one can tell from the (risk) ratios, boiled or baked fish is in the protective direction but not fried fish.”
The findings also suggest that the cardioprotective benefits vary by gender and ethnicity — perhaps because of the preparation methods, genetic susceptibility or hormonal factors.
Many studies have suggested that eating omega-3 fatty acids reduces the risk of heart disease; however, little is known about which source is most beneficial.
In this study, researchers examined the source, type, amount and frequency of dietary omega-3 ingestion among gender and ethnic groups. Participants were part of the Multiethnic Cohort living in Hawaii and Los Angeles County when they were recruited between 1993 and 1996. The group consisted of 82,243 men and 103,884 women of African-American, Caucasian, Japanese, Native Hawaiian and Latino descent ages 45 to 75 years old with no history of heart disease.
Researchers divided their intake of canned tuna, other canned fish, fish excluding shell fish, or soy products that contain plant omega-3s (soy, tofu and shoyu) into quintiles, quartiles, or tertiles when applicable. They also surveyed the preparation methods: raw, baked, boiled; fried; salted or dried. The initial study did not consider grilled fish.
Those in the highest quintile consumed a median 3.3 grams of omega-3 fatty acids a day. The lowest quintile consumed a median of 0.8 grams a day.
Omega-3 intake was inversely associated with overall risk of death due to heart disease in men — a trend mainly observed in Caucasians, Japanese Americans and Latinos. However, there weren’t many blacks or Hawaiians in the study, so the results should be interpreted cautiously, Meng said.
Overall, men who ate about 3.3 grams per day of omega-3 fatty acids had a 23 percent lower risk of cardiac death compared to those who ate 0.8 grams daily.
“Clearly, we are seeing that the higher the dietary omega-3 intake, the lower the risk of dying from heart disease among men,” Meng said.
Japanese and Hawaiians eat fish more often compared to whites, blacks and Latinos, and they prepare fish in a variety of methods, Meng noted.
For women, the omega-3 effect was cardioprotective at each level of consumption but not consistently significant, Meng said. Salted and dried fish was a risk factor in women.
In contrast, adding less than 1.1 gram/day shoyu and teriyaki sauce at the dinner table was protective for men but not for greater than 1.1 gram/day. For women, shoyu use showed a clear inverse relationship to death from heart disease. She noted that shoyu that is high in sodium can raise blood pressure, so she stressed low-sodium products. Eating tofu also had a cardioprotective effect in all ethnic groups.
“My guess is that, for women, eating omega-3s from shoyu and tofu that contain other active ingredients such as phytoestrogens, might have a stronger cardioprotective effect than eating just omega-3s,” said Meng, noting that further studies are needed to confirm the hypothesis.
During the average 11.9 years of follow-up, 4,516 heart-related deaths occurred in the group, according to state and national death records, which were cross-referenced through the end of 2005.
The study didn’t consider possible dietary changes over time; subjects who were diagnosed with heart disease after their baseline food intake surveys might have modified their eating habits. Further, the study didn’t account for the possible effects of fish-oil supplementation.
In light of these limitations, the researchers plan to include subjects’ dietary patterns over time and a cross-validation of their omega-3 levels through blood analysis.
“Our findings can help educate people on how much fish to eat and how to cook it to prevent heart disease,” Meng said. “Alternately, if it is verified that the interactions between fish consumption, risk factors and ethnicity are due to genetic susceptibility, the heart-disease prevention message can be personalized to ethnic groups, and future study could identify susceptibility at the genetic level.”
The American Heart Association recommends eating fish (particularly fatty fish) at least two times a week and eating tofu and other forms of soybeans, canola, walnut and flaxseed, and their oils. Learn specific information on the recommendations.
Acetaminophen (Tylenol)=Liver Damage w/o Vit. U
Common herbal medicine may prevent acetaminophen-related liver damage, says Stanford researcher
"I didn't know anything about the substance that was necessary for the pathway's function, so I had to look it up," said Gary Peltz, MD, PhD, professor of anesthesiology. "My postdoctoral fellow, whose parents and other family members in Asia were taking this compound in their supplements, started laughing. He recognized it immediately."
Acetaminophen is a pain reliever present in many over-the-counter cold and flu medicines, especially Tylenol. It is broken down, or metabolized, in the body into byproducts — one of which can be very toxic to the liver. At normal, therapeutic levels, this byproduct is easily deactivated when it binds to a naturally occurring, protective molecule called glutathione. But the body's glutathione stores are finite, and are quickly depleted when the recommended doses of acetaminophen are exceeded.
Unfortunately, the prevalence of acetaminophen makes it easy to accidentally exceed the recommended levels, which can occur by dosing more frequently than indicated or by combining two or more acetaminophen-containing products. However, severe liver damage can occur at even two to three times the recommended dose (the maximum adult dose is 4 grams per day; toxic daily levels range from 7 to 10 grams).
"It's a huge public health problem," said Peltz. "It's particularly difficult for parents, who may not realize that acetaminophen is in so many pediatric medicines." Acetaminophen overdose is the most common cause of liver transplantation in this country. The only effective antidote is an unpalatable compound called NAC that can induce nausea and vomiting, and must be administered as soon as possible after the overdose.
A well-known Eastern medicine supplement may help avoid the most common cause of liver transplantation, according to a study by researchers at the Stanford University School of Medicine. The finding came as a surprise to the scientists, who used a number of advanced genetic and genomic techniques in mice to identify a molecular pathway that counters acetaminophen toxicity, which leads to liver failure.
The molecule was S-methylmethionine, which had been marketed as an herbal medicine known as Vitamin U for treatment of the digestive system. It is highly abundant in many plants, including cabbage and wheat, and is routinely ingested by people.
Peltz and his colleagues used 16 inbred strains of laboratory mice for their investigations. Most strains are susceptible to acetaminophen toxicity, but one is resistant. They compared how the drug is metabolized by the different strains and looked for variations in gene expression and changes in endogenous metabolites in response to acetaminophen administration. They identified 224 candidate genes that might explain the resistant strain's ability to ward off liver damage, and then plumbed computer databases to identify those involved in metabolizing acetaminophen's dangerous byproducts.
One, an enzyme called Bhmt2, fit the bill: It helped generate more glutathione, and its sequence varied between the resistant and non-resistant strains of mice. Bhmt2 works by converting the diet-derived molecule S-methylmethionine, or SMM, into methionine, which is subsequently converted in a series of steps into glutathione. The researchers confirmed the importance of the pathway by showing that SMM conferred protection against acetaminophen-induced liver toxicity only in strains of mice in which the Bhmt2 pathway was functional.
"By administering SMM, which is found in every flowering plant and vegetable, we were able to prevent a lot of the drug's toxic effect," said Peltz. He and his colleagues are now working to set up clinical trials at Stanford to see whether it will have a similar effect in humans. In the meantime, though, he cautions against assuming that dosing oneself with SMM will protect against acetaminophen overdose.
"There are many pathways involved in the metabolism of this drug, and individuals' genetic backgrounds are tremendously variable. This is just one piece of the puzzle; we don't have the full answer," he said. However, if subsequent studies are promising, Peltz envisions possibly a co-formulated drug containing both acetaminophen and SMM or using SMM as a routine dietary supplement.
"I didn't know anything about the substance that was necessary for the pathway's function, so I had to look it up," said Gary Peltz, MD, PhD, professor of anesthesiology. "My postdoctoral fellow, whose parents and other family members in Asia were taking this compound in their supplements, started laughing. He recognized it immediately."
Acetaminophen is a pain reliever present in many over-the-counter cold and flu medicines, especially Tylenol. It is broken down, or metabolized, in the body into byproducts — one of which can be very toxic to the liver. At normal, therapeutic levels, this byproduct is easily deactivated when it binds to a naturally occurring, protective molecule called glutathione. But the body's glutathione stores are finite, and are quickly depleted when the recommended doses of acetaminophen are exceeded.
Unfortunately, the prevalence of acetaminophen makes it easy to accidentally exceed the recommended levels, which can occur by dosing more frequently than indicated or by combining two or more acetaminophen-containing products. However, severe liver damage can occur at even two to three times the recommended dose (the maximum adult dose is 4 grams per day; toxic daily levels range from 7 to 10 grams).
"It's a huge public health problem," said Peltz. "It's particularly difficult for parents, who may not realize that acetaminophen is in so many pediatric medicines." Acetaminophen overdose is the most common cause of liver transplantation in this country. The only effective antidote is an unpalatable compound called NAC that can induce nausea and vomiting, and must be administered as soon as possible after the overdose.
A well-known Eastern medicine supplement may help avoid the most common cause of liver transplantation, according to a study by researchers at the Stanford University School of Medicine. The finding came as a surprise to the scientists, who used a number of advanced genetic and genomic techniques in mice to identify a molecular pathway that counters acetaminophen toxicity, which leads to liver failure.
The molecule was S-methylmethionine, which had been marketed as an herbal medicine known as Vitamin U for treatment of the digestive system. It is highly abundant in many plants, including cabbage and wheat, and is routinely ingested by people.
Peltz and his colleagues used 16 inbred strains of laboratory mice for their investigations. Most strains are susceptible to acetaminophen toxicity, but one is resistant. They compared how the drug is metabolized by the different strains and looked for variations in gene expression and changes in endogenous metabolites in response to acetaminophen administration. They identified 224 candidate genes that might explain the resistant strain's ability to ward off liver damage, and then plumbed computer databases to identify those involved in metabolizing acetaminophen's dangerous byproducts.
One, an enzyme called Bhmt2, fit the bill: It helped generate more glutathione, and its sequence varied between the resistant and non-resistant strains of mice. Bhmt2 works by converting the diet-derived molecule S-methylmethionine, or SMM, into methionine, which is subsequently converted in a series of steps into glutathione. The researchers confirmed the importance of the pathway by showing that SMM conferred protection against acetaminophen-induced liver toxicity only in strains of mice in which the Bhmt2 pathway was functional.
"By administering SMM, which is found in every flowering plant and vegetable, we were able to prevent a lot of the drug's toxic effect," said Peltz. He and his colleagues are now working to set up clinical trials at Stanford to see whether it will have a similar effect in humans. In the meantime, though, he cautions against assuming that dosing oneself with SMM will protect against acetaminophen overdose.
"There are many pathways involved in the metabolism of this drug, and individuals' genetic backgrounds are tremendously variable. This is just one piece of the puzzle; we don't have the full answer," he said. However, if subsequent studies are promising, Peltz envisions possibly a co-formulated drug containing both acetaminophen and SMM or using SMM as a routine dietary supplement.
Folic Acid = Increased Risk of Cancer, Death
Patients with heart disease in Norway, a country with no fortification of foods with folic acid, had an associated increased risk of cancer and death from any cause if they had received treatment with folic acid and vitamin B12, according to a study in the November 18 issue of JAMA.
Most epidemiological studies have found inverse associations between folate (a B vitamin) intake and risk of colorectal cancer, although such associations have been inconsistent or absent for other cancers, according to background information in the article. “Experimental evidence suggests that folate deficiency may promote initial stages of carcinogenesis, whereas high doses of folic acid may enhance growth of cancer cells. Since 1998, many countries, including the United States, have implemented mandatory folic acid fortification of flour and grain products to reduce the risk of neural-tube birth defects,” the authors write. “Recently, concerns have emerged about the safety of folic acid, in particular with respect to cancer risk.”
Marta Ebbing, M.D., of Haukeland University Hospital, Bergen, Norway, and colleagues analyzed the results of two Norwegian homocysteine-lowering trials among patients with ischemic heart disease, where there was a statistically nonsignificant increase in cancer incidence in the groups assigned to folic acid treatment. The researchers examined whether folic acid treatment was associated with cancer outcomes and all-cause mortality after extended follow-up. “Because there is no folic acid fortification of foods in Norway, this study population was well suited for such an investigation,” they write.
The two randomized, placebo-controlled clinical trials included 6,837 patients with ischemic heart disease who were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007. Patients were randomized to receive oral treatment with folic acid (0.8 mg/d), plus vitamin B12 (0.4 mg/d), plus vitamin B6 (40 mg/d) (n = 1,708); folic acid (0.8 mg/d) plus vitamin B12 (0.4 mg/d) (n = 1,703); vitamin B6 alone (40 mg/d) (n = 1,705); or placebo (n = 1,721). During study treatment, median (midpoint) serum folate concentration increased more than 6-fold among participants given folic acid.
The researchers found that after a median 39 months of treatment and an additional 38 months of post-trial observational follow-up, 288 participants (8.4 percent) who did not receive folic acid plus vitamin B12 vs. 341 participants (10.0 percent) who received such treatment were diagnosed with cancer, a 21 percent increased risk. A total of 100 patients (2.9 percent) who did not receive folic acid plus vitamin B12 vs. 136 (4.0 percent) who received such treatment died from cancer, a 38 percent increased risk. A total of 16.1 percent of patients who received folic acid plus vitamin B12 vs. 13.8 percent who did not receive such treatment died from any cause.
“Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B12. Vitamin B6 treatment was not associated with any significant effects,” the authors write.
“Our results need confirmation in other populations and underline the call for safety monitoring following the widespread consumption of folic acid from dietary supplements and fortified foods.”
Most epidemiological studies have found inverse associations between folate (a B vitamin) intake and risk of colorectal cancer, although such associations have been inconsistent or absent for other cancers, according to background information in the article. “Experimental evidence suggests that folate deficiency may promote initial stages of carcinogenesis, whereas high doses of folic acid may enhance growth of cancer cells. Since 1998, many countries, including the United States, have implemented mandatory folic acid fortification of flour and grain products to reduce the risk of neural-tube birth defects,” the authors write. “Recently, concerns have emerged about the safety of folic acid, in particular with respect to cancer risk.”
Marta Ebbing, M.D., of Haukeland University Hospital, Bergen, Norway, and colleagues analyzed the results of two Norwegian homocysteine-lowering trials among patients with ischemic heart disease, where there was a statistically nonsignificant increase in cancer incidence in the groups assigned to folic acid treatment. The researchers examined whether folic acid treatment was associated with cancer outcomes and all-cause mortality after extended follow-up. “Because there is no folic acid fortification of foods in Norway, this study population was well suited for such an investigation,” they write.
The two randomized, placebo-controlled clinical trials included 6,837 patients with ischemic heart disease who were treated with B vitamins or placebo between 1998 and 2005, and were followed up through December 31, 2007. Patients were randomized to receive oral treatment with folic acid (0.8 mg/d), plus vitamin B12 (0.4 mg/d), plus vitamin B6 (40 mg/d) (n = 1,708); folic acid (0.8 mg/d) plus vitamin B12 (0.4 mg/d) (n = 1,703); vitamin B6 alone (40 mg/d) (n = 1,705); or placebo (n = 1,721). During study treatment, median (midpoint) serum folate concentration increased more than 6-fold among participants given folic acid.
The researchers found that after a median 39 months of treatment and an additional 38 months of post-trial observational follow-up, 288 participants (8.4 percent) who did not receive folic acid plus vitamin B12 vs. 341 participants (10.0 percent) who received such treatment were diagnosed with cancer, a 21 percent increased risk. A total of 100 patients (2.9 percent) who did not receive folic acid plus vitamin B12 vs. 136 (4.0 percent) who received such treatment died from cancer, a 38 percent increased risk. A total of 16.1 percent of patients who received folic acid plus vitamin B12 vs. 13.8 percent who did not receive such treatment died from any cause.
“Results were mainly driven by increased lung cancer incidence in participants who received folic acid plus vitamin B12. Vitamin B6 treatment was not associated with any significant effects,” the authors write.
“Our results need confirmation in other populations and underline the call for safety monitoring following the widespread consumption of folic acid from dietary supplements and fortified foods.”
Monday, November 16, 2009
CPR - chest compression alone better
Continuous chest compression-CPR improved cardiac arrest survival in Arizona
Statewide analysis shows bystanders can save more lives when doing chest compressions only instead of mouth-to-mouth CPR
The chance of surviving a cardiac arrest outside a hospital was found to be twice as high when bystanders performed continuous chest compressions without mouth-to-mouth breathing than when bystanders performed standard CPR. These are the latest findings reported by the Resuscitation Research Group at the University of Arizona Sarver Heart Center and the SHARE Program (Save Hearts in Arizona Research and Education) at the Arizona Department of Health Services.
Only 5 percent of cardiac arrest victims survived if nobody performed CPR. In those receiving standard CPR (alternating between 30 compressions and 2 breaths), survival was marginally higher at 6 percent. In contrast, 11 percent survived if bystanders kept pumping on their chest and did not stop for mouth-to-mouth breaths until emergency medical services arrived. These trends were even more pronounced in those patients facing the highest survival chance to begin with due to the specific nature of their cardiac arrest, namely those whose collapse was witnessed and whose heart was in a rhythm that is most likely to respond to a shock from a defibrillator. In those, the survival rate was 17 percent without bystander CPR, 19 percent with standard CPR and 32 percent with continuous chest compressions.
The analysis also showed that while the percentage of bystanders administering CPR increased only slightly over the past four years, of those that did choose to help, 77 percent opted for chest compressions without mouth-to-mouth breathing instead of standard CPR. Before, that number was only 16 percent.
The results of the analysis, which included 4,850 out-of-hospital cardiac arrests in Arizona that occurred from 2005 and 2009, will be presented by Gordon A. Ewy, MD, director of the UA Sarver Heart Center at the "Best of the Best" abstract session of the American Heart Association's Resuscitation Symposium in Orlando, Fla., on Sunday, Nov. 15 at 5pm.
"Over the course of three days, out-of-hospital cardiac arrest claims as many lives in the U.S. as the September 11 attacks," Dr. Ewy said. "This study is the first to show that bystanders can raise the odds of survival by giving continuous chest compressions rather than the type of CPR they are being taught in most certification classes. If we can get more people to act, more patients who were on the brink of death will be walking out of the hospital neurologically intact."
Bentley J. Bobrow, MD, medical director of the Bureau of Emergency Medical Services & Trauma System at the Arizona Department of Health Services, said: "All previously published reports only showed that bystander CPR was better than not doing any CPR until the paramedics arrive, and that early CPR resulted in better survival than late CPR. Our statewide efforts promoting Compression-Only CPR have resulted in significantly improved survival rates for patients in out-of-hospital cardiac arrest."
Statewide analysis shows bystanders can save more lives when doing chest compressions only instead of mouth-to-mouth CPR
The chance of surviving a cardiac arrest outside a hospital was found to be twice as high when bystanders performed continuous chest compressions without mouth-to-mouth breathing than when bystanders performed standard CPR. These are the latest findings reported by the Resuscitation Research Group at the University of Arizona Sarver Heart Center and the SHARE Program (Save Hearts in Arizona Research and Education) at the Arizona Department of Health Services.
Only 5 percent of cardiac arrest victims survived if nobody performed CPR. In those receiving standard CPR (alternating between 30 compressions and 2 breaths), survival was marginally higher at 6 percent. In contrast, 11 percent survived if bystanders kept pumping on their chest and did not stop for mouth-to-mouth breaths until emergency medical services arrived. These trends were even more pronounced in those patients facing the highest survival chance to begin with due to the specific nature of their cardiac arrest, namely those whose collapse was witnessed and whose heart was in a rhythm that is most likely to respond to a shock from a defibrillator. In those, the survival rate was 17 percent without bystander CPR, 19 percent with standard CPR and 32 percent with continuous chest compressions.
The analysis also showed that while the percentage of bystanders administering CPR increased only slightly over the past four years, of those that did choose to help, 77 percent opted for chest compressions without mouth-to-mouth breathing instead of standard CPR. Before, that number was only 16 percent.
The results of the analysis, which included 4,850 out-of-hospital cardiac arrests in Arizona that occurred from 2005 and 2009, will be presented by Gordon A. Ewy, MD, director of the UA Sarver Heart Center at the "Best of the Best" abstract session of the American Heart Association's Resuscitation Symposium in Orlando, Fla., on Sunday, Nov. 15 at 5pm.
"Over the course of three days, out-of-hospital cardiac arrest claims as many lives in the U.S. as the September 11 attacks," Dr. Ewy said. "This study is the first to show that bystanders can raise the odds of survival by giving continuous chest compressions rather than the type of CPR they are being taught in most certification classes. If we can get more people to act, more patients who were on the brink of death will be walking out of the hospital neurologically intact."
Bentley J. Bobrow, MD, medical director of the Bureau of Emergency Medical Services & Trauma System at the Arizona Department of Health Services, said: "All previously published reports only showed that bystander CPR was better than not doing any CPR until the paramedics arrive, and that early CPR resulted in better survival than late CPR. Our statewide efforts promoting Compression-Only CPR have resulted in significantly improved survival rates for patients in out-of-hospital cardiac arrest."
Transcendental Med=less heart attack,stroke,death
Patients with coronary heart disease who practiced the stress-reducing Transcendental Meditation® technique had nearly 50 percent lower rates of heart attack, stroke, and death compared to nonmeditating controls, according to the results of a first-ever study presented during the annual meeting of the American Heart Association in Orlando, Fla., on Nov.16, 2009.
The trial was sponsored by a $3.8 million grant from the National Institutes of Health–National Heart, Lung, and Blood Institute, and was conducted at The Medical College of Wisconsin in Milwaukee in collaboration with the Institute for Natural Medicine and Prevention at Maharishi University of Management in Fairfield, Iowa.
The nine-year, randomized control trial followed 201African American men and women, average age 59 years, with narrowing of arteries in their hearts who were randomly assigned to either practice the stress-reducing Transcendental Meditation technique or to participate in a control group which received health education classes in traditional risk factors, including dietary modification and exercise.
All participants continued standard medications and other usual medical care.
The study found:
A 47 percent reduction in the combination of death, heart attacks, and strokes in the participants
Clinically significant (5 mm Hg average) reduction in blood pressure associated with decrease in clinical events
Significant reductions in psychological stress in the high-stress subgroup
According to Robert Schneider, M.D., FACC, lead author and director of the Center for Natural Medicine and Prevention, "Previous research on Transcendental Meditation has shown reductions in blood pressure, psychological stress, and other risk factors for heart disease, irrespective of ethnicity. But this is the first controlled clinical trial to show that long-term practice of this particular stress reduction program reduces the incidence of clinical cardiovascular events, that is heart attacks, strokes and mortality."
"This study is an example of the contribution of a lifestyle intervention—stress management—to the prevention of cardiovascular disease in high-risk patients," said Theodore Kotchen, M.D., co-author of the study, professor of medicine, and associate dean for clinical research at the Medical College. Other investigators at the Milwaukee site included Drs. Jane Kotchen and Clarence Grim.
Dr. Schneider said that the effect of Transcendental Meditation in the trial was like adding a class of newly discovered medications for the prevention of heart disease. "In this case, the new medications are derived from the body's own internal pharmacy stimulated by the Transcendental Meditation practice," he said.
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Fast Facts on Coronary Heart Disease
Coronary heart disease (CHD) is the leading cause of death in the United States
There are nearly 1.5 million heart attacks per year in the US, according to the American Heart Association
An American will suffer a heart attack every 34 seconds
Coronary heart disease is also the leading cause of health care costs. More than $475 billion is spent annually on treating CHD, including:
$100,000 for each coronary bypass surgery
$50,000 for each angioplasty
$30,000 for each diagnostic cardiac catheterization
There are nearly 500,000 coronary artery bypass grafts and 1.3 million angioplasties performed every year
Stress is thought to contribute to the development of CHD
The trial was sponsored by a $3.8 million grant from the National Institutes of Health–National Heart, Lung, and Blood Institute, and was conducted at The Medical College of Wisconsin in Milwaukee in collaboration with the Institute for Natural Medicine and Prevention at Maharishi University of Management in Fairfield, Iowa.
The nine-year, randomized control trial followed 201African American men and women, average age 59 years, with narrowing of arteries in their hearts who were randomly assigned to either practice the stress-reducing Transcendental Meditation technique or to participate in a control group which received health education classes in traditional risk factors, including dietary modification and exercise.
All participants continued standard medications and other usual medical care.
The study found:
A 47 percent reduction in the combination of death, heart attacks, and strokes in the participants
Clinically significant (5 mm Hg average) reduction in blood pressure associated with decrease in clinical events
Significant reductions in psychological stress in the high-stress subgroup
According to Robert Schneider, M.D., FACC, lead author and director of the Center for Natural Medicine and Prevention, "Previous research on Transcendental Meditation has shown reductions in blood pressure, psychological stress, and other risk factors for heart disease, irrespective of ethnicity. But this is the first controlled clinical trial to show that long-term practice of this particular stress reduction program reduces the incidence of clinical cardiovascular events, that is heart attacks, strokes and mortality."
"This study is an example of the contribution of a lifestyle intervention—stress management—to the prevention of cardiovascular disease in high-risk patients," said Theodore Kotchen, M.D., co-author of the study, professor of medicine, and associate dean for clinical research at the Medical College. Other investigators at the Milwaukee site included Drs. Jane Kotchen and Clarence Grim.
Dr. Schneider said that the effect of Transcendental Meditation in the trial was like adding a class of newly discovered medications for the prevention of heart disease. "In this case, the new medications are derived from the body's own internal pharmacy stimulated by the Transcendental Meditation practice," he said.
###
Fast Facts on Coronary Heart Disease
Coronary heart disease (CHD) is the leading cause of death in the United States
There are nearly 1.5 million heart attacks per year in the US, according to the American Heart Association
An American will suffer a heart attack every 34 seconds
Coronary heart disease is also the leading cause of health care costs. More than $475 billion is spent annually on treating CHD, including:
$100,000 for each coronary bypass surgery
$50,000 for each angioplasty
$30,000 for each diagnostic cardiac catheterization
There are nearly 500,000 coronary artery bypass grafts and 1.3 million angioplasties performed every year
Stress is thought to contribute to the development of CHD
Low Vitamin D = stroke, heart disease and death
Study finds inadequate levels of Vitamin D may significantly increase risk of stroke, heart disease and death
While mothers have known that feeding their kids milk builds strong bones, a new study by researchers at the Heart Institute at Intermountain Medical Center in Salt Lake City suggests that Vitamin D contributes to a strong and healthy heart as well – and that inadequate levels of the vitamin may significantly increase a person's risk of stroke, heart disease, and death, even among people who've never had heart disease.
For more than a year, the Intermountain Medical Center research team followed 27,686 patients who were 50 years of age or older with no prior history of cardiovascular disease. The participants had their blood Vitamin D levels tested during routine clinical care. The patients were divided into three groups based on their Vitamin D levels – normal (over 30 nanograms per milliliter), low (15-30 ng/ml), or very low (less than 15 ng/ml). The patients were then followed to see if they developed some form of heart disease.
Researchers found that patients with very low levels of Vitamin D were 77 percent more likely to die, 45 percent more likely to develop coronary artery disease, and 78 percent were more likely to have a stroke than patients with normal levels. Patients with very low levels of Vitamin D were also twice as likely to develop heart failure than those with normal Vitamin D levels.
Findings from the study will be presented at the American Heart Association's Scientific Conference on Monday, Nov. 16 in Orlando, Florida.
"This was a unique study because the association between Vitamin D deficiency and cardiovascular disease has not been well-established," says Brent Muhlestein, MD, director of cardiovascular research of the Heart Institute at Intermountain Medical Center and one of the authors of the new study. "Its conclusions about how we can prevent disease and provide treatment may ultimately help us save more lives."
A wealth of research has already shown that Vitamin D is involved in the body's regulation of calcium, which strengthens bones — and as a result, its deficiency is associated with musculoskeletal disorders. Recently, studies have also linked Vitamin D to the regulation of many other bodily functions including blood pressure, glucose control, and inflammation, all of which are important risk factors related to heart disease. From these results, scientists have postulated that Vitamin D deficiency may also be linked to heart disease itself.
"Utah's population gave us a unique pool of patients whose health histories are different than patients in previous studies," Dr. Muhlestein says. "For example, because of Utah's low use of tobacco and alcohol, we were able to narrow the focus of the study to the effects of Vitamin D on the cardiovascular system."
The results were quite surprising and very important, says Heidi May, PhD, MS, an epidemiologist with the Intermountain Medical Center research team and one of the study authors.
"We concluded that among patients 50 years of age or older, even a moderate deficiency of Vitamin D levels was associated with developing coronary artery disease, heart failure, stroke, and death," she says. "This is important because Vitamin D deficiency is easily treated. If increasing levels of Vitamin D can decrease some risk associated with these cardiovascular diseases, it could have a significant public health impact. When you consider that cardiovascular disease is the leading cause of death in America, you understand how this research can help improve the length and quality of people's lives."
Because the study was only observational, definitive links between Vitamin D deficiency and heart disease could not be assigned — but the findings create an impetus for further study, says Dr. Muhlestein.
"We believe the findings are important enough to now justify randomized treatment trials of supplementation in patients with Vitamin D deficiency to determine for sure whether it can reduce the risk of heart disease," he says.
Zinc reduces dangerous cystein
Judging from the number of juices and teas advertised as containing antioxidants, consumers are aware of the dangers of oxidative stress. But what is the best way to measure it – and fight it?
Doctors at Emory University School of Medicine have identified a substance in the blood that may be useful in predicting an individual's risk for heart disease. The substance is cystine, an oxidized form of the amino acid cysteine and an indirect measure of oxidative stress.
In a study of more than 1,200 people undergoing cardiac imaging at Emory because of suspected heart disease, people with high levels of cystine in the blood were twice as likely to have a heart attack or die over the next few years.
Riyaz Patel, MD, a postdoctoral researcher at Emory's Cardiovascular Research Group, is presenting the results Monday at the American Heart Association Scientific Sessions meeting in Orlando.
Patel was part of a team led by Arshed Quyyumi, MD, professor of medicine (cardiology) at Emory University School of Medicine.
When considered independently of variables such as the presence of diabetes, high levels of cystine still predicted future trouble, Patel says. In the current research, high levels means the quarter of the group of patients with the highest levels.
"Cystine could be a valuable marker of cardiovascular risk, but it also has a direct harmful effect on cells, so reducing it may be a valuable treatment strategy," he says. "What's exciting is there are already known ways to intervene and drive down cystine levels in patients."
For example, a previous study has shown that supplementing the diet with zinc can lower cystine levels, he says.
Several studies have shown that levels of oxidized cysteine in the blood tend to rise as people age. Smoking and alcohol consumption are also linked with higher levels of oxidized cysteine.
Cysteine is itself a short-lived precursor to glutathione, one of the main antioxidants found inside cells, says Dean P. Jones, PhD, professor of medicine and director of the Clinical Biomarkers Laboratory at Emory University School of Medicine.
"We need to have a continuous supply of cysteine, but it is too reactive for us to have very much at any one time," he says. "We are not sure why the oxidized form of cysteine accumulates with aging and disease. But our studies show that when it accumulates, it activates inflammation in cells."
Jones and his colleagues have shown that when white blood cells are exposed to high levels of cystine, they display signs of inflammation and become stickier. That makes them more likely to adhere to blood vessels in the heart, an event that contributes to the development of heart disease.
The team has found that levels of cystine do not correlate with C-reactive protein, a blood marker of inflammation other scientists have studied for a possible relationship with heart disease. The team's future plans include comparing cystine to other markers of inflammation and understanding the relationships between them.
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More about cysteine and oxidative stress.
Doctors at Emory University School of Medicine have identified a substance in the blood that may be useful in predicting an individual's risk for heart disease. The substance is cystine, an oxidized form of the amino acid cysteine and an indirect measure of oxidative stress.
In a study of more than 1,200 people undergoing cardiac imaging at Emory because of suspected heart disease, people with high levels of cystine in the blood were twice as likely to have a heart attack or die over the next few years.
Riyaz Patel, MD, a postdoctoral researcher at Emory's Cardiovascular Research Group, is presenting the results Monday at the American Heart Association Scientific Sessions meeting in Orlando.
Patel was part of a team led by Arshed Quyyumi, MD, professor of medicine (cardiology) at Emory University School of Medicine.
When considered independently of variables such as the presence of diabetes, high levels of cystine still predicted future trouble, Patel says. In the current research, high levels means the quarter of the group of patients with the highest levels.
"Cystine could be a valuable marker of cardiovascular risk, but it also has a direct harmful effect on cells, so reducing it may be a valuable treatment strategy," he says. "What's exciting is there are already known ways to intervene and drive down cystine levels in patients."
For example, a previous study has shown that supplementing the diet with zinc can lower cystine levels, he says.
Several studies have shown that levels of oxidized cysteine in the blood tend to rise as people age. Smoking and alcohol consumption are also linked with higher levels of oxidized cysteine.
Cysteine is itself a short-lived precursor to glutathione, one of the main antioxidants found inside cells, says Dean P. Jones, PhD, professor of medicine and director of the Clinical Biomarkers Laboratory at Emory University School of Medicine.
"We need to have a continuous supply of cysteine, but it is too reactive for us to have very much at any one time," he says. "We are not sure why the oxidized form of cysteine accumulates with aging and disease. But our studies show that when it accumulates, it activates inflammation in cells."
Jones and his colleagues have shown that when white blood cells are exposed to high levels of cystine, they display signs of inflammation and become stickier. That makes them more likely to adhere to blood vessels in the heart, an event that contributes to the development of heart disease.
The team has found that levels of cystine do not correlate with C-reactive protein, a blood marker of inflammation other scientists have studied for a possible relationship with heart disease. The team's future plans include comparing cystine to other markers of inflammation and understanding the relationships between them.
##
More about cysteine and oxidative stress.
Broccoli and cauliflower protect cells from damage
Scientists at the University of Pennsylvania School of Medicine discovered that a dietary antioxidant found in such vegetables as broccoli and cauliflower protects cells from damage caused by chemicals generated during the body’s inflammatory response to infection and injury. The finding has implications for such inflammation-based disorders as cystic fibrosis (CF), diabetes, heart disease, and neurodegeneration.
Through cell-culture studies and a synthesis of known antioxidant biochemistry, Zhe Lu, MD, PhD , Professor of Physiology, Yanping Xu , MD, PhD , Senior Research Investigator, and Szilvia Szép , PhD, postdoctoral researcher, showed that the antioxidant thiocyanate normally existing in the body protects lung cells from injuries caused by accumulations of hydrogen peroxide and hypochlorite, the active ingredient in household bleach. These potentially harmful chemicals are made by the body as a reaction to infection and injury. In addition, thiocyanate also protects cells from hypochlorite produced in reactions involving MPO, an enzyme released from germ-fighting white blood cells during inflammation. They published their finding this week in the Proceedings of the National Academy of Sciences. Lu is also an Investigator of the Howard Hughes Medical Institute.
“Dr. Lu’s work throws new light on how the genetic defect underlying CF leads to the lung illnesses that are the leading cause of death,” said Bert Shapiro, Ph.D., who oversees membrane structure grants at the National Institutes of Health’s National Institute of General Medical Sciences (NIGMS). “His team’s findings suggest that the lungs of people with the disease are more susceptible to the damaging effects of cellular oxidants. While the idea is tantalizing and creative, further testing is needed to confirm it.”
The research team demonstrated that in three additional cell types used to extend their ideas to other inflammation-related conditions – cardiovascular disease, neurodegeneration, and diabetes – thiocyanate at blood concentrations of at least 100 micromolar (micromoles per liter) greatly reduces the toxicity of MPO in cells, including those lining blood vessels. Humans naturally derive thiocyanate from some vegetables and blood levels of thiocyanate in the general population vary from 10 to 140 micromolar.
This comparison raises the possibility, the authors point out, that without an adequate dietary supply of thiocyanate, hypochlorite produced by the body during inflammation would cause additional collateral damage to cells, thus worsening inflammatory diseases, and predisposing humans to diseases linked to MPO activity, including atherosclerosis.
Connection to CF
For over a decade Lu and colleagues have been exploring the inner workings of ion channels and how this knowledge relates to the pathology of such diseases as CF. The CF disease originates from mutations in the CF transmembrane conductance regulator (CFTR) protein, an ion channel protein in the cell membrane commonly thought to transport mainly chloride ions. It has, however, remained a mystery why a defect in a chloride-transporting channel leads to cystic fibrosis, a disease with exaggerated inflammation in both the lungs and the digestive system.
Lung injuries inflicted by excessive inflammation and recurring infection cause about ninety percent of CF patients’ symptoms and mortality. Although known as a chloride channel, CFTR also conducts thiocyanate ions, important because, in several ways, they can limit potentially harmful accumulations of hydrogen peroxide and hypochlorite, chemicals produced by the body to fight germs.
In CF patients, there is also a high incidence of diabetes, partly caused by damage to the pancreas. Type 2 diabetes is also associated with higher levels of MPO in the blood. The researchers found that the MPO-caused injuries to pancreas cells and endothelial cells used in their experiments can be greatly reduced by as little as 100 micromolar thiocyanate. Their finding raises the possibility that MPO, in the absence of adequate thiocyanate, contributes to diabetes.
In the cell-based experiments, thiocyanate at concentrations below 100 micromolar did not eliminate hypochlorite accumulation and did not fully protect against MPO toxicity. Conceivably, inadequate thiocyanate levels would aggravate MPO-produced injuries in patients suffering from inflammatory diseases, surmise the authors.
Links to Other Diseases
In other studies, MPO activity has been linked to lung cancers among smokers and also implicated in neurodegenerative diseases. Intriguingly, people with congenital MPO deficiency are less likely to develop cardiovascular diseases. The research team found that MPO-caused injuries to nerve cells, as well as to blood vessel-lining endothelial cells, can be greatly reduced by 100 micromolar thiocyanate.
Genetic defects in the CFTR predispose CF patients’ lungs to excessive inflammation entangled with recurring lung infection. Defective CFTR channels would be expected to result in lower thiocyanate concentrations in the affected regions within the respiratory, as well as the digestive systems, leaving tissues inadequately protected from accumulated hydrogen peroxide and overproduced hypochlorite.
Conceptually, delivering thiocyanate directly to the digestive and respiratory systems might be a therapy for CF disease, propose the researchers. As for the general population, individuals with low blood levels of thiocyanate may be at risk for chronic injuries by MPO, predisposing them to inflammatory or inflammation-mediated diseases. Many investigators have proposed developing drugs that specifically inhibit MPO-catalyzed hypochlorite production to combat these diseases, but natural thiocyanate not only decreases MPO-catalyzed formation of hypochlorite but also rapidly, once it is made, neutralizes it.
“In light of the obvious implications of this protective action of thiocyanate against the cell-damaging effect of MPO activity with regard to both CF disease and general population health, my colleagues and I will vigorously investigate the potential health benefit of thiocyanate,” says Lu. He emphasizes though, “until the research community acquires a better understanding of both positive and negative impacts of thiocyanate on human health, it would be unwise for anyone to self-administer thiocyanate because like many other chemicals, thiocyanate has adverse side effects at improper doses and/or under inappropriate conditions.
Through cell-culture studies and a synthesis of known antioxidant biochemistry, Zhe Lu, MD, PhD , Professor of Physiology, Yanping Xu , MD, PhD , Senior Research Investigator, and Szilvia Szép , PhD, postdoctoral researcher, showed that the antioxidant thiocyanate normally existing in the body protects lung cells from injuries caused by accumulations of hydrogen peroxide and hypochlorite, the active ingredient in household bleach. These potentially harmful chemicals are made by the body as a reaction to infection and injury. In addition, thiocyanate also protects cells from hypochlorite produced in reactions involving MPO, an enzyme released from germ-fighting white blood cells during inflammation. They published their finding this week in the Proceedings of the National Academy of Sciences. Lu is also an Investigator of the Howard Hughes Medical Institute.
“Dr. Lu’s work throws new light on how the genetic defect underlying CF leads to the lung illnesses that are the leading cause of death,” said Bert Shapiro, Ph.D., who oversees membrane structure grants at the National Institutes of Health’s National Institute of General Medical Sciences (NIGMS). “His team’s findings suggest that the lungs of people with the disease are more susceptible to the damaging effects of cellular oxidants. While the idea is tantalizing and creative, further testing is needed to confirm it.”
The research team demonstrated that in three additional cell types used to extend their ideas to other inflammation-related conditions – cardiovascular disease, neurodegeneration, and diabetes – thiocyanate at blood concentrations of at least 100 micromolar (micromoles per liter) greatly reduces the toxicity of MPO in cells, including those lining blood vessels. Humans naturally derive thiocyanate from some vegetables and blood levels of thiocyanate in the general population vary from 10 to 140 micromolar.
This comparison raises the possibility, the authors point out, that without an adequate dietary supply of thiocyanate, hypochlorite produced by the body during inflammation would cause additional collateral damage to cells, thus worsening inflammatory diseases, and predisposing humans to diseases linked to MPO activity, including atherosclerosis.
Connection to CF
For over a decade Lu and colleagues have been exploring the inner workings of ion channels and how this knowledge relates to the pathology of such diseases as CF. The CF disease originates from mutations in the CF transmembrane conductance regulator (CFTR) protein, an ion channel protein in the cell membrane commonly thought to transport mainly chloride ions. It has, however, remained a mystery why a defect in a chloride-transporting channel leads to cystic fibrosis, a disease with exaggerated inflammation in both the lungs and the digestive system.
Lung injuries inflicted by excessive inflammation and recurring infection cause about ninety percent of CF patients’ symptoms and mortality. Although known as a chloride channel, CFTR also conducts thiocyanate ions, important because, in several ways, they can limit potentially harmful accumulations of hydrogen peroxide and hypochlorite, chemicals produced by the body to fight germs.
In CF patients, there is also a high incidence of diabetes, partly caused by damage to the pancreas. Type 2 diabetes is also associated with higher levels of MPO in the blood. The researchers found that the MPO-caused injuries to pancreas cells and endothelial cells used in their experiments can be greatly reduced by as little as 100 micromolar thiocyanate. Their finding raises the possibility that MPO, in the absence of adequate thiocyanate, contributes to diabetes.
In the cell-based experiments, thiocyanate at concentrations below 100 micromolar did not eliminate hypochlorite accumulation and did not fully protect against MPO toxicity. Conceivably, inadequate thiocyanate levels would aggravate MPO-produced injuries in patients suffering from inflammatory diseases, surmise the authors.
Links to Other Diseases
In other studies, MPO activity has been linked to lung cancers among smokers and also implicated in neurodegenerative diseases. Intriguingly, people with congenital MPO deficiency are less likely to develop cardiovascular diseases. The research team found that MPO-caused injuries to nerve cells, as well as to blood vessel-lining endothelial cells, can be greatly reduced by 100 micromolar thiocyanate.
Genetic defects in the CFTR predispose CF patients’ lungs to excessive inflammation entangled with recurring lung infection. Defective CFTR channels would be expected to result in lower thiocyanate concentrations in the affected regions within the respiratory, as well as the digestive systems, leaving tissues inadequately protected from accumulated hydrogen peroxide and overproduced hypochlorite.
Conceptually, delivering thiocyanate directly to the digestive and respiratory systems might be a therapy for CF disease, propose the researchers. As for the general population, individuals with low blood levels of thiocyanate may be at risk for chronic injuries by MPO, predisposing them to inflammatory or inflammation-mediated diseases. Many investigators have proposed developing drugs that specifically inhibit MPO-catalyzed hypochlorite production to combat these diseases, but natural thiocyanate not only decreases MPO-catalyzed formation of hypochlorite but also rapidly, once it is made, neutralizes it.
“In light of the obvious implications of this protective action of thiocyanate against the cell-damaging effect of MPO activity with regard to both CF disease and general population health, my colleagues and I will vigorously investigate the potential health benefit of thiocyanate,” says Lu. He emphasizes though, “until the research community acquires a better understanding of both positive and negative impacts of thiocyanate on human health, it would be unwise for anyone to self-administer thiocyanate because like many other chemicals, thiocyanate has adverse side effects at improper doses and/or under inappropriate conditions.
Deficiencies in vitamin D = hardened arteries
Heart and Bone Damage From Low Vitamin D Tied to Declines in Sex Hormones; Effects of Vitamin D Deficiency Amplified by Shortage of Estrogen
Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone.
In a national study in 1010 men, to be presented Nov. 15 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando (Poster Abstract #20601a, Poster Hall A2-A3, Orange County Convention Center, Orlando, Fla.), researchers say the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened and narrowed arteries and weakened bones. Vitamin D is an essential part to keeping the body healthy, and can be obtained from fortified foods, such as milk and cereals, and by exposure to sunlight.
"Our results confirm a long-suspected link and suggest that vitamin D supplements, which are already prescribed to treat osteoporosis, may also be useful in preventing heart disease," says lead study investigator and cardiologist Erin Michos, M.D., M.H.S.
"All three steroid hormones - vitamin D, estrogen and testosterone - are produced from cholesterol, whose blood levels are known to influence arterial and bone health," says Michos, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "Our study gives us a much better understanding of how the three work in concert to affect cardiovascular and bone health."
Michos says the overall biological relationship continues to puzzle scientists because studies of the long-term effects of adding estrogen in the form of hormone replacement therapy in women failed to show fewer deaths from heart disease. Indeed, results showed that in some women, an actual increase in heart disease and stroke rates occurred, although, bone fractures declined.
The Hopkins team's latest data were provided by analyzing blood samples from a subset of men participating in a study on cancer. That study was part of a larger, ongoing national health survey involving both men and women and was designed to compare the risk of diseases between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 20 nanograms per milliliter or lower.
The men in the study had their hormone levels measured for both chemical forms of testosterone and estrogen found in blood, when each is either unattached or circulating freely, and when each is attached to a separate protein, known as sex hormone binding globulin, or SHBG for short.
Initial results showed no link between vitamin D deficiency and depressed blood levels of either hormone. And despite finding a harmful relationship between depressed testosterone levels and rates of heart disease, stroke, and high blood pressure, as well as osteopenia in men, researchers found that it was independent of deficiencies in vitamin D.
However, when researchers compared ratios of estrogen to SHBG levels, they found that rates of both diseases, especially osteopenia, the early stage of osteoporosis, were higher when both estrogen and vitamin D levels were depressed.
For every single unit decrease in ratios of estrogen to SHBG (both in nanomoles per liter), men low in vitamin D showed an 89 percent increase in osteopenia, but men with sufficient vitamin D levels had a less worrisome 64 percent jump.
Using the same measure of estrogen levels, men low in vitamin D were also at heightened risk of cardiovascular diseases, at 12 percent, compared to men with adequate levels of the vitamin, at 1 percent, numbers that researchers say are still statistically significant.
"These results reinforce the message of how important proper quantities of vitamin D are to good bone health, and that a man's risk of developing osteoporosis and heart disease is heavily weighted on the complex and combined interaction of how any such vitamin deficits interact with both their sex hormones, in particular, estrogen," Michos says.
Michos and her team next plan to analyze blood samples from women to see if the same results from men hold true.
Michos recommends that men and women boost their vitamin D levels by eating diets rich in fatty fish, such as cod, sardines and mackerel, consuming fortified dairy products, taking vitamin supplements, and in warmer weather briefly exposing skin to the sun's vitamin-D producing ultraviolet light.
She points out that clinical trials are under way to determine whether or not vitamin D supplements can prevent incidents of or deaths from heart attack, stroke and other signs of cardiovascular disease.
The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units, but Michos feels this is inadequate to achieve optimal nutrient blood levels (above 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.
Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone.
In a national study in 1010 men, to be presented Nov. 15 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando (Poster Abstract #20601a, Poster Hall A2-A3, Orange County Convention Center, Orlando, Fla.), researchers say the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened and narrowed arteries and weakened bones. Vitamin D is an essential part to keeping the body healthy, and can be obtained from fortified foods, such as milk and cereals, and by exposure to sunlight.
"Our results confirm a long-suspected link and suggest that vitamin D supplements, which are already prescribed to treat osteoporosis, may also be useful in preventing heart disease," says lead study investigator and cardiologist Erin Michos, M.D., M.H.S.
"All three steroid hormones - vitamin D, estrogen and testosterone - are produced from cholesterol, whose blood levels are known to influence arterial and bone health," says Michos, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "Our study gives us a much better understanding of how the three work in concert to affect cardiovascular and bone health."
Michos says the overall biological relationship continues to puzzle scientists because studies of the long-term effects of adding estrogen in the form of hormone replacement therapy in women failed to show fewer deaths from heart disease. Indeed, results showed that in some women, an actual increase in heart disease and stroke rates occurred, although, bone fractures declined.
The Hopkins team's latest data were provided by analyzing blood samples from a subset of men participating in a study on cancer. That study was part of a larger, ongoing national health survey involving both men and women and was designed to compare the risk of diseases between those with the lowest blood levels of vitamin D to those with higher amounts. An unhealthy deficiency, experts say, is considered blood levels of 20 nanograms per milliliter or lower.
The men in the study had their hormone levels measured for both chemical forms of testosterone and estrogen found in blood, when each is either unattached or circulating freely, and when each is attached to a separate protein, known as sex hormone binding globulin, or SHBG for short.
Initial results showed no link between vitamin D deficiency and depressed blood levels of either hormone. And despite finding a harmful relationship between depressed testosterone levels and rates of heart disease, stroke, and high blood pressure, as well as osteopenia in men, researchers found that it was independent of deficiencies in vitamin D.
However, when researchers compared ratios of estrogen to SHBG levels, they found that rates of both diseases, especially osteopenia, the early stage of osteoporosis, were higher when both estrogen and vitamin D levels were depressed.
For every single unit decrease in ratios of estrogen to SHBG (both in nanomoles per liter), men low in vitamin D showed an 89 percent increase in osteopenia, but men with sufficient vitamin D levels had a less worrisome 64 percent jump.
Using the same measure of estrogen levels, men low in vitamin D were also at heightened risk of cardiovascular diseases, at 12 percent, compared to men with adequate levels of the vitamin, at 1 percent, numbers that researchers say are still statistically significant.
"These results reinforce the message of how important proper quantities of vitamin D are to good bone health, and that a man's risk of developing osteoporosis and heart disease is heavily weighted on the complex and combined interaction of how any such vitamin deficits interact with both their sex hormones, in particular, estrogen," Michos says.
Michos and her team next plan to analyze blood samples from women to see if the same results from men hold true.
Michos recommends that men and women boost their vitamin D levels by eating diets rich in fatty fish, such as cod, sardines and mackerel, consuming fortified dairy products, taking vitamin supplements, and in warmer weather briefly exposing skin to the sun's vitamin-D producing ultraviolet light.
She points out that clinical trials are under way to determine whether or not vitamin D supplements can prevent incidents of or deaths from heart attack, stroke and other signs of cardiovascular disease.
The U.S. Institute of Medicine suggests that an adequate daily intake of vitamin D is between 200 and 400 international units, but Michos feels this is inadequate to achieve optimal nutrient blood levels (above 30 nanograms per milliliter). Previous results from the same nationwide survey showed that 41 percent of men and 53 percent of women are technically deficient in the nutrient, with vitamin D levels below 28 nanograms per milliliter.
Niacin - Blood Cholesterol Levels Improved
Vitamin B Niacin - Blood Cholesterol Levels Improved, But Arteries Do Not Show It
There were promising gains in bad (LDL) and good (HDL) blood cholesterol levels in those taking niacin. Results showed that in the group taking both niacin and a statin, blood levels of LDL-cholesterol fell 5 percent more than in the group taking only statin medications. And levels of HDL jumped 14 percent more than in the statin-only group.
However, there was no extra benefit in correcting arterial narrowing and diminishing plaque buildup in seniors who already have coronary artery disease, a new vascular imaging study from Johns Hopkins experts shows.
In tests on 145 Baltimore-area men and women with existing atherosclerosis, all over age 65, researchers found that after 18 months of drug therapy, reductions in arterial wall thickness were measurably no different between the half who took dual niacin-statin therapy and the rest who remained on statin therapy alone.
The results were the same whether they took any one of the three leading statin medications: atorvastatin (Lipitor), simvistatin (Zocor) or rosuvastatin (Crestor). Seniors on dual drug therapy had an average 5.4 cubic millimeter per month scale back in plaque buildup in the main neck artery, while those taking just a cholesterol-lowering statin medication came down by 4 cubic millimeters per month, a difference that researchers say is not statistically significant.
The team will present its findings Nov. 18 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando (Abstract #16424, Room #W202, Orange County Convention Center).
According to senior study investigator and Johns Hopkins cardiologist João Lima, M.D., the lack of any discernible advantage occurred
"Our findings tell us that improved cholesterol levels from taking combination vitamin B niacin and statin therapy do not necessarily translate into observable benefits in reversing and stalling carotid artery disease," says Lima, a professor of medicine and radiology at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "This does not mean that niacin therapy may not have other cardiovascular benefits, but any such benefits are independent of reducing the amount of plaque buildup and patients should be aware of that."
"Our recommendation to physicians is that current national treatment guidelines, which recommend mainly statin therapy tailored to the severity of atherosclerosis for preventing arteries from reclogging and narrowing, appear to be sufficient and accurate for physicians and patients to follow," says Lima.
However, Lima cautions that an ongoing national study of the long-term vascular benefits of dual therapy and whether extended-release niacin, also known as nicotinic acid, lowers death rates from heart disease should provide more definitive data. Hopkins is participating in that research, as well. He also notes that extended-releases niacin used in this study is a prescription medication, and that it is not sold over the counter like many other vitamin B products.
"The real value in initially studying this particular group of people is that these seniors are the ones who I am most likely to see in the hospital, the group most vulnerable to coronary artery disease and most at risk of suffering an arterial blockage, heart attack, or stroke," says lead study investigator Christopher Sibley, M.D. Nearly 17 million American adults are estimated to have some form of coronary artery disease, resulting in more than 400,000 deaths each year.
"Practically speaking, carotid MRI scans are an option to assess the risk of patients based on the amount of plaque in their arteries, to better determine who needs aggressive statin therapy and to monitor how well they respond to treatment," says Sibley, an adjunct assistant professor at Johns Hopkins, as well as a staff clinician at the National Institutes of Health Clinical Center.
All study participants had one or more preexisting cardiovascular health issues, such as a previous heart attack, stroke, coronary artery bypass grafting to resupply blood to the heart, severe chest pain, or angioplasty with the placement of wire stents to keep arteries open.
At the start of the study, participants received an MRI scan of their carotid artery, and again every six months thereafter. The four sets of carotid images provided what Sibley says is "an important window" into what is going on in the body's network of veins and arteries. He notes that the neck artery is important not just because it serves as the main blood supply to the brain, but also because narrowing in the carotid artery reflects the risk of future heart attack.
Sibley says that the team has begun to analyze blood samples collected as part of the study, searching for chemicals that might also signal a change in arterial plaque buildup and progressive arterial narrowing.
There were promising gains in bad (LDL) and good (HDL) blood cholesterol levels in those taking niacin. Results showed that in the group taking both niacin and a statin, blood levels of LDL-cholesterol fell 5 percent more than in the group taking only statin medications. And levels of HDL jumped 14 percent more than in the statin-only group.
However, there was no extra benefit in correcting arterial narrowing and diminishing plaque buildup in seniors who already have coronary artery disease, a new vascular imaging study from Johns Hopkins experts shows.
In tests on 145 Baltimore-area men and women with existing atherosclerosis, all over age 65, researchers found that after 18 months of drug therapy, reductions in arterial wall thickness were measurably no different between the half who took dual niacin-statin therapy and the rest who remained on statin therapy alone.
The results were the same whether they took any one of the three leading statin medications: atorvastatin (Lipitor), simvistatin (Zocor) or rosuvastatin (Crestor). Seniors on dual drug therapy had an average 5.4 cubic millimeter per month scale back in plaque buildup in the main neck artery, while those taking just a cholesterol-lowering statin medication came down by 4 cubic millimeters per month, a difference that researchers say is not statistically significant.
The team will present its findings Nov. 18 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando (Abstract #16424, Room #W202, Orange County Convention Center).
According to senior study investigator and Johns Hopkins cardiologist João Lima, M.D., the lack of any discernible advantage occurred
"Our findings tell us that improved cholesterol levels from taking combination vitamin B niacin and statin therapy do not necessarily translate into observable benefits in reversing and stalling carotid artery disease," says Lima, a professor of medicine and radiology at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "This does not mean that niacin therapy may not have other cardiovascular benefits, but any such benefits are independent of reducing the amount of plaque buildup and patients should be aware of that."
"Our recommendation to physicians is that current national treatment guidelines, which recommend mainly statin therapy tailored to the severity of atherosclerosis for preventing arteries from reclogging and narrowing, appear to be sufficient and accurate for physicians and patients to follow," says Lima.
However, Lima cautions that an ongoing national study of the long-term vascular benefits of dual therapy and whether extended-release niacin, also known as nicotinic acid, lowers death rates from heart disease should provide more definitive data. Hopkins is participating in that research, as well. He also notes that extended-releases niacin used in this study is a prescription medication, and that it is not sold over the counter like many other vitamin B products.
"The real value in initially studying this particular group of people is that these seniors are the ones who I am most likely to see in the hospital, the group most vulnerable to coronary artery disease and most at risk of suffering an arterial blockage, heart attack, or stroke," says lead study investigator Christopher Sibley, M.D. Nearly 17 million American adults are estimated to have some form of coronary artery disease, resulting in more than 400,000 deaths each year.
"Practically speaking, carotid MRI scans are an option to assess the risk of patients based on the amount of plaque in their arteries, to better determine who needs aggressive statin therapy and to monitor how well they respond to treatment," says Sibley, an adjunct assistant professor at Johns Hopkins, as well as a staff clinician at the National Institutes of Health Clinical Center.
All study participants had one or more preexisting cardiovascular health issues, such as a previous heart attack, stroke, coronary artery bypass grafting to resupply blood to the heart, severe chest pain, or angioplasty with the placement of wire stents to keep arteries open.
At the start of the study, participants received an MRI scan of their carotid artery, and again every six months thereafter. The four sets of carotid images provided what Sibley says is "an important window" into what is going on in the body's network of veins and arteries. He notes that the neck artery is important not just because it serves as the main blood supply to the brain, but also because narrowing in the carotid artery reflects the risk of future heart attack.
Sibley says that the team has begun to analyze blood samples collected as part of the study, searching for chemicals that might also signal a change in arterial plaque buildup and progressive arterial narrowing.
Migraine Raises Risk of Most Common Form of Stroke
Migraine Raises Risk of Most Common Form of Stroke; Women More at Risk Than Men; Risk Particularly High in Those With Visual Symptoms
Pooling results from 21 studies, involving 622,381 men and women, researchers at Johns Hopkins have affirmed that migraine headaches are associated with more than twofold higher chances of the most common kind of stroke: those occurring when blood supply to the brain is suddenly cut off by the buildup of plaque or a blood clot.
The risk for those with migraines is 2.3 times those without, according to calculations from the Johns Hopkins team, to be presented Nov. 16 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando. (Abstract #21106, Poster Hall A2-A3, Orange County Convention Center, Orlando, Fla.) For those who experience aura, the sighting of flashing lights, zigzag lines and blurred side vision along with migraines, the risk of so-called ischemic stroke is 2.5 times higher, and in women, 2.9 times as high.
Study participants, mostly in North America and Europe, were between the ages 18 and 70, and none had suffered a stroke prior to enrollment.
Senior study investigator and cardiologist Saman Nazarian, M.D., says the team's latest analysis, believed to be the largest study of its kind on the topic, reinforces the relationship between migraine and stroke while correcting some discrepancies in previous analyses. For examples, a smaller combination study in 2005 by researchers in Montreal showed a bare doubling of risk, yet mixed together different mathematical measures of risk, while the Hopkins study kept them separate, pooling together only like measures. As well, another half dozen recent and smaller studies from Harvard University yielded mixed results, some showing a link between migraines and ischemic stroke, while one did not show a tie-in.
Nazarian says that while nearly 1,800 articles have been written about the relationship between migraine and ischemic stroke, the Hopkins review was more selective, combining only studies with similar designs and similar groups of people, and more comprehensive, including analysis of unpublished data.
"Identifying people at highest risk is crucial to preventing disabling strokes," says Nazarian, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "Based on this data, physicians should consider addressing stroke risk factors in patients with a history or signs of light flashes and blurry vision associated with severe headaches."
Prevention and treatment options for migraine, he says, range from smoking cessation and taking anti-blood pressure or blood-thinning medications, such as aspirin. In women with migraines, stopping use of oral contraceptives or hormone replacement therapy may be recommended.
Such widespread use of hormone-controlling drugs is what Nazarian says may explain why women with migraines have such high risk of ischemic stroke.
Contraceptives and other estrogen therapies are both known to contribute to long-term risk factors for cardiovascular diseases and stroke, such as high blood pressure and increased reactivity by clot-forming blood platelets.
Nazarian says the researchers' next steps are to evaluate if preventive therapies, especially aspirin, offset the risk of ischemic stroke in people with migraines.
Pooling results from 21 studies, involving 622,381 men and women, researchers at Johns Hopkins have affirmed that migraine headaches are associated with more than twofold higher chances of the most common kind of stroke: those occurring when blood supply to the brain is suddenly cut off by the buildup of plaque or a blood clot.
The risk for those with migraines is 2.3 times those without, according to calculations from the Johns Hopkins team, to be presented Nov. 16 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando. (Abstract #21106, Poster Hall A2-A3, Orange County Convention Center, Orlando, Fla.) For those who experience aura, the sighting of flashing lights, zigzag lines and blurred side vision along with migraines, the risk of so-called ischemic stroke is 2.5 times higher, and in women, 2.9 times as high.
Study participants, mostly in North America and Europe, were between the ages 18 and 70, and none had suffered a stroke prior to enrollment.
Senior study investigator and cardiologist Saman Nazarian, M.D., says the team's latest analysis, believed to be the largest study of its kind on the topic, reinforces the relationship between migraine and stroke while correcting some discrepancies in previous analyses. For examples, a smaller combination study in 2005 by researchers in Montreal showed a bare doubling of risk, yet mixed together different mathematical measures of risk, while the Hopkins study kept them separate, pooling together only like measures. As well, another half dozen recent and smaller studies from Harvard University yielded mixed results, some showing a link between migraines and ischemic stroke, while one did not show a tie-in.
Nazarian says that while nearly 1,800 articles have been written about the relationship between migraine and ischemic stroke, the Hopkins review was more selective, combining only studies with similar designs and similar groups of people, and more comprehensive, including analysis of unpublished data.
"Identifying people at highest risk is crucial to preventing disabling strokes," says Nazarian, an assistant professor at the Johns Hopkins University School of Medicine and its Heart and Vascular Institute. "Based on this data, physicians should consider addressing stroke risk factors in patients with a history or signs of light flashes and blurry vision associated with severe headaches."
Prevention and treatment options for migraine, he says, range from smoking cessation and taking anti-blood pressure or blood-thinning medications, such as aspirin. In women with migraines, stopping use of oral contraceptives or hormone replacement therapy may be recommended.
Such widespread use of hormone-controlling drugs is what Nazarian says may explain why women with migraines have such high risk of ischemic stroke.
Contraceptives and other estrogen therapies are both known to contribute to long-term risk factors for cardiovascular diseases and stroke, such as high blood pressure and increased reactivity by clot-forming blood platelets.
Nazarian says the researchers' next steps are to evaluate if preventive therapies, especially aspirin, offset the risk of ischemic stroke in people with migraines.
Saturday, November 14, 2009
Too much selenium can increase your cholesterol
A new study from the University of Warwick has discovered taking too much of the essential mineral selenium in your diet can increase your cholesterol by almost 10%.
Selenium is a trace essential mineral with anti-oxidant properties. The body naturally absorbs selenium from foods such as vegetables, meat and seafood. However, when the balance is altered and the body absorbs too much selenium, such as through taking selenium supplements, it can have adverse affects.
A team led by Dr Saverio Stranges at the University's Warwick Medical School has found high levels of selenium are associated with increased cholesterol, which can cause heart disease.
In a paper recently published in the Journal of Nutrition, the research team examined the association of plasma selenium concentrations (levels of selenium in the blood) with blood lipids (fats in the blood).
The researchers found in those participants with higher plasma selenium (more than 1.20 µmol/L) there was an average total cholesterol level increase of 8% (0.39 mmol/L (i.e. 15.1 mg/dL). Researchers also noted a 10% increase in non-HDL cholesterol levels (lipoproteins within your total cholesterol that can help predict the risk of someone suffering a heart attack or chest pain). Also, of the participants with the highest selenium levels, 48.2% admitted they regularly took dietary supplements.
The study was conducted among 1042 participants aged 19-64 in the 2000-2001 UK National Diet and Nutrition Survey. All participants were interviewed face-to-face to assess lifestyle factors such as diet and drinking habits. Blood samples were then taken for analysis.
Dr Saverio Stranges said although high selenium levels were not exclusively caused by people taking dietary supplements, the results of the study were concerning because the use of selenium dietary supplements had risen considerably in the UK in recent years. He said this was largely due to the perception that selenium can reduce the risk of cancer and other diseases.
He said: “This use has spread despite a lack of definitive evidence on selenium supplements efficacy for cancer and other chronic disease prevention. The cholesterol increases we have identified may have important implications for public health. In fact, such a difference could translate into a large number of premature deaths from coronary heart disease.
“We believe that the widespread use of selenium supplements, or of any other strategy that artificially increases selenium status above the level required is unwarranted at the present time. Further research is needed to examine the full range of health effects of increased selenium, whether beneficial or detrimental.”
Selenium is a trace essential mineral with anti-oxidant properties. The body naturally absorbs selenium from foods such as vegetables, meat and seafood. However, when the balance is altered and the body absorbs too much selenium, such as through taking selenium supplements, it can have adverse affects.
A team led by Dr Saverio Stranges at the University's Warwick Medical School has found high levels of selenium are associated with increased cholesterol, which can cause heart disease.
In a paper recently published in the Journal of Nutrition, the research team examined the association of plasma selenium concentrations (levels of selenium in the blood) with blood lipids (fats in the blood).
The researchers found in those participants with higher plasma selenium (more than 1.20 µmol/L) there was an average total cholesterol level increase of 8% (0.39 mmol/L (i.e. 15.1 mg/dL). Researchers also noted a 10% increase in non-HDL cholesterol levels (lipoproteins within your total cholesterol that can help predict the risk of someone suffering a heart attack or chest pain). Also, of the participants with the highest selenium levels, 48.2% admitted they regularly took dietary supplements.
The study was conducted among 1042 participants aged 19-64 in the 2000-2001 UK National Diet and Nutrition Survey. All participants were interviewed face-to-face to assess lifestyle factors such as diet and drinking habits. Blood samples were then taken for analysis.
Dr Saverio Stranges said although high selenium levels were not exclusively caused by people taking dietary supplements, the results of the study were concerning because the use of selenium dietary supplements had risen considerably in the UK in recent years. He said this was largely due to the perception that selenium can reduce the risk of cancer and other diseases.
He said: “This use has spread despite a lack of definitive evidence on selenium supplements efficacy for cancer and other chronic disease prevention. The cholesterol increases we have identified may have important implications for public health. In fact, such a difference could translate into a large number of premature deaths from coronary heart disease.
“We believe that the widespread use of selenium supplements, or of any other strategy that artificially increases selenium status above the level required is unwarranted at the present time. Further research is needed to examine the full range of health effects of increased selenium, whether beneficial or detrimental.”
Friday, November 13, 2009
Soy, Coffee=+ for Colon Cancer/- for Breast Cancer
A compound in coffee has been found to be estrogenic in studies by Texas AgriLife Research scientists.
Though the studies have not been conducted to determine recommended consumption amounts, scientists say the compound, called trigonelline or "trig," may be a factor in estrogen-dependent breast cancer but beneficial against colon cancer development.
"The important thing to get from this is that 'trig' has the ability to act like a hormone," said Dr. Clinton Allred, AgriLife Research nutrition scientist. "So there is a tie to cancer in the sense that we are looking at estrogen-dependent cancer cells. But that doesn't suggest that it would actually cause the disease. I don't believe there should be any concern about drinking coffee at this point."
His report was published in the Journal of Nutrition. Allred's lab studies dietary compounds that can mimic the hormone estradiol – the primary hormone in women. His main focus has been to look at how estrogen protects against the development of colon cancer. Estradiol is one of three estrogen hormones. "There's a history of these compounds in crops such as soy," Allred said. "Soy has a number of different compounds that actually can mimic estradiol in several disease states some of which are good and some of which have the potential to be more deleterious-type effects."
Allred said a former colleague mentioned an interest in finding the properties of "trig" – a natural compound used in traditional Indian culture for post-menopausal women.
Because the chemical structure of "trig" was so unlike estradiol, Allred didn't think the compound would be estrogenic.
"Estrogen-dependent tumors in the presence of estradiol will grow faster," Allred said. "If you use those cells in a laboratory setting, you can determine whether something is estrogenic because they will literally make a tumor grow faster."
He said that a series of experiences and different approaches showed that "trig," a vitamin derivative, was fairly estrogenic at very low concentrations.
"We haven't gotten as far as to suggest that if a woman had the disease that it would necessarily be a problem. But what we've proven is that the compound is estrogenic or can be at certain concentrations and doses," Allred said.
He added that "trig" is in coffee beans, though in different amounts depending on the variety of coffee bean. The two major types of coffee beans used for what is consumed in the U.S. both contain it, he said.
"The more you roast a coffee bean, the less there is," Allred said. "But the most critical aspect is that when you do a water extract of ground coffee, which is basically how you make a cup of coffee. It does in fact come out in the water, so we know it is in a cup of coffee."
Nevertheless, the researchers have no idea what the exposure level would be or whether a particularly exposure – say from one cup of coffee – would be in the range seen in the laboratory tests.
"It is way too early to say that drinking a cup of coffee is exposing you to something that is definitely going to be estrogenic. All we know is that there is a compound in there that can be estrogenic in our systems. That is really the take-home message," Allred said.
Allred also cautioned that people often narrow one compound in a food without considering the total mix of compounds and how they interact with each other or in a human body.
"There is never a single compound when you're looking at food, and a cup of coffee is a food," Allred said. "There's a whole bunch of other things in it. There's caffeine. There's actually a little bit of fat. There are all sorts of others things in a cup of coffee that could interact with this."
The numerous compounds in each food product means there are complex interactions, he explained, which is why nutritionists advise people that the whole food is better than any individual compound.
"That's why you can't take supplements to make up for food. You can never take all the things that are in a carrot and replace a carrot. In the end, you need to eat the carrot," he said. "We're a long way from understanding what this compound could do in the context of a food."
He said a concern is that menopausal women seek over-the-counter phytoestrogen compounds to relieve symptoms such as hot flashes. Women want what they believe to be a natural and/or safe mechanism, he said, because hormone replacement therapy has such a negative connotation.
But, Allred said, researchers estimate that from the time an estrogen-dependent breast tumor begins until it is diagnosed in a woman is about 30 years.
"That means there will be a number of women out there who will become menopausal, and begin to take phytoestrogens in supplement form," he said. "The majority of those come from soy. So our concern was, what if a woman becomes menopausal which means her estrogen levels are going to be low, she has estrogen-dependent breast cancer and doesn't even know it. And now she's consuming phytoestrogens.
"Physicians would never recommend you be on hormone replacement therapy if you had estrogen-dependent cancer. From a toxicology standpoint, it would that be a bad thing if you were consuming these phytoestrogens in high enough doses. It could be really dangerous."
A problem is that people believe that natural or plant-derived compounds are automatically safe which is not necessarily always true, he said. Also, consuming a compound in its pure form as a supplement in high doses may not be healthy.
"If we were getting a hormone from an animal, you wouldn't see people do that," he said. "The only difference is that this is a plant-derived compound, so they feel it is safe when that may not be so."
Yet, Allred added, scientists are finding that at least some of these compounds are doing positive things to prevent colon cancer.
"So there's going to be places that it's good – just as we've seen with estradiol," he noted. "There are going to be some disease states that it is quite good for and some disease states that you need to be mindful of."
Still, the compound's potential as a weapon against colon cancer has the researchers "pretty excited about that."
"We're seeing very interesting information as far as tumor formation and the ability of phytoestrogens to prevent colon cancer formation. So any other new, natural phytoestrogen that we are able to identify and relate to the diet, that would be the model we'd bring it in to," Allred said of possible future studies on "trig."
He said a hope would be to develop a drug that could treat colon tissue without getting into the entire body, thus exploiting the compound's mechanism to protect again cancer formation without producing other estrogenic effects.
"It's really important for us to come up with strategies that we can have the benefits in the colon without the risks associated with (estrogenic compounds)," Allred said.
Though the studies have not been conducted to determine recommended consumption amounts, scientists say the compound, called trigonelline or "trig," may be a factor in estrogen-dependent breast cancer but beneficial against colon cancer development.
"The important thing to get from this is that 'trig' has the ability to act like a hormone," said Dr. Clinton Allred, AgriLife Research nutrition scientist. "So there is a tie to cancer in the sense that we are looking at estrogen-dependent cancer cells. But that doesn't suggest that it would actually cause the disease. I don't believe there should be any concern about drinking coffee at this point."
His report was published in the Journal of Nutrition. Allred's lab studies dietary compounds that can mimic the hormone estradiol – the primary hormone in women. His main focus has been to look at how estrogen protects against the development of colon cancer. Estradiol is one of three estrogen hormones. "There's a history of these compounds in crops such as soy," Allred said. "Soy has a number of different compounds that actually can mimic estradiol in several disease states some of which are good and some of which have the potential to be more deleterious-type effects."
Allred said a former colleague mentioned an interest in finding the properties of "trig" – a natural compound used in traditional Indian culture for post-menopausal women.
Because the chemical structure of "trig" was so unlike estradiol, Allred didn't think the compound would be estrogenic.
"Estrogen-dependent tumors in the presence of estradiol will grow faster," Allred said. "If you use those cells in a laboratory setting, you can determine whether something is estrogenic because they will literally make a tumor grow faster."
He said that a series of experiences and different approaches showed that "trig," a vitamin derivative, was fairly estrogenic at very low concentrations.
"We haven't gotten as far as to suggest that if a woman had the disease that it would necessarily be a problem. But what we've proven is that the compound is estrogenic or can be at certain concentrations and doses," Allred said.
He added that "trig" is in coffee beans, though in different amounts depending on the variety of coffee bean. The two major types of coffee beans used for what is consumed in the U.S. both contain it, he said.
"The more you roast a coffee bean, the less there is," Allred said. "But the most critical aspect is that when you do a water extract of ground coffee, which is basically how you make a cup of coffee. It does in fact come out in the water, so we know it is in a cup of coffee."
Nevertheless, the researchers have no idea what the exposure level would be or whether a particularly exposure – say from one cup of coffee – would be in the range seen in the laboratory tests.
"It is way too early to say that drinking a cup of coffee is exposing you to something that is definitely going to be estrogenic. All we know is that there is a compound in there that can be estrogenic in our systems. That is really the take-home message," Allred said.
Allred also cautioned that people often narrow one compound in a food without considering the total mix of compounds and how they interact with each other or in a human body.
"There is never a single compound when you're looking at food, and a cup of coffee is a food," Allred said. "There's a whole bunch of other things in it. There's caffeine. There's actually a little bit of fat. There are all sorts of others things in a cup of coffee that could interact with this."
The numerous compounds in each food product means there are complex interactions, he explained, which is why nutritionists advise people that the whole food is better than any individual compound.
"That's why you can't take supplements to make up for food. You can never take all the things that are in a carrot and replace a carrot. In the end, you need to eat the carrot," he said. "We're a long way from understanding what this compound could do in the context of a food."
He said a concern is that menopausal women seek over-the-counter phytoestrogen compounds to relieve symptoms such as hot flashes. Women want what they believe to be a natural and/or safe mechanism, he said, because hormone replacement therapy has such a negative connotation.
But, Allred said, researchers estimate that from the time an estrogen-dependent breast tumor begins until it is diagnosed in a woman is about 30 years.
"That means there will be a number of women out there who will become menopausal, and begin to take phytoestrogens in supplement form," he said. "The majority of those come from soy. So our concern was, what if a woman becomes menopausal which means her estrogen levels are going to be low, she has estrogen-dependent breast cancer and doesn't even know it. And now she's consuming phytoestrogens.
"Physicians would never recommend you be on hormone replacement therapy if you had estrogen-dependent cancer. From a toxicology standpoint, it would that be a bad thing if you were consuming these phytoestrogens in high enough doses. It could be really dangerous."
A problem is that people believe that natural or plant-derived compounds are automatically safe which is not necessarily always true, he said. Also, consuming a compound in its pure form as a supplement in high doses may not be healthy.
"If we were getting a hormone from an animal, you wouldn't see people do that," he said. "The only difference is that this is a plant-derived compound, so they feel it is safe when that may not be so."
Yet, Allred added, scientists are finding that at least some of these compounds are doing positive things to prevent colon cancer.
"So there's going to be places that it's good – just as we've seen with estradiol," he noted. "There are going to be some disease states that it is quite good for and some disease states that you need to be mindful of."
Still, the compound's potential as a weapon against colon cancer has the researchers "pretty excited about that."
"We're seeing very interesting information as far as tumor formation and the ability of phytoestrogens to prevent colon cancer formation. So any other new, natural phytoestrogen that we are able to identify and relate to the diet, that would be the model we'd bring it in to," Allred said of possible future studies on "trig."
He said a hope would be to develop a drug that could treat colon tissue without getting into the entire body, thus exploiting the compound's mechanism to protect again cancer formation without producing other estrogenic effects.
"It's really important for us to come up with strategies that we can have the benefits in the colon without the risks associated with (estrogenic compounds)," Allred said.
Exercise lowers risk of stroke and cancer
1. Physical exercise prevents stroke. In men, exercise lowers the risk of cerebral hemorrhage by 40%, and that of cerebral infarction by 27%. Rapid walking or cycling suffices to achieve this effect. In women, a statistically significant effect has not been demonstrated.
http://www.aerzteblatt.de/v4/archiv/pdf.asp?id=66574
2. Regular walking lowers the risk of colorectal carcinoma by 40%. Patients with colorectal carcinoma can also improve their prognosis by exercising.
http://www.aerzteblatt.de/v4/archiv/pdf.asp?id=66575
http://www.aerzteblatt.de/v4/archiv/pdf.asp?id=66574
2. Regular walking lowers the risk of colorectal carcinoma by 40%. Patients with colorectal carcinoma can also improve their prognosis by exercising.
http://www.aerzteblatt.de/v4/archiv/pdf.asp?id=66575
Wednesday, November 11, 2009
Dark chocolate helps ease emotional stress
The "chocolate cure" for emotional stress is getting new support from a clinical trial published online in ACS' Journal of Proteome Research. It found that eating about an ounce and a half of dark chocolate a day for two weeks reduced levels of stress hormones in the bodies of people feeling highly stressed. Everyone's favorite treat also partially corrected other stress-related biochemical imbalances.
Sunil Kochhar and colleagues note growing scientific evidence that antioxidants and other beneficial substances in dark chocolate may reduce risk factors for heart disease and other physical conditions. Studies also suggest that chocolate may ease emotional stress. Until now, however, there was little evidence from research in humans on exactly how chocolate might have those stress-busting effects.
In the study, scientists identified reductions in stress hormones and other stress-related biochemical changes in volunteers who rated themselves as highly stressed and ate dark chocolate for two weeks. "The study provides strong evidence that a daily consumption of 40 grams [1.4 ounces] during a period of 2 weeks is sufficient to modify the metabolism of healthy human volunteers," the scientists say.
"Metabolic Effects of Dark Chocolate Consumption on Energy, Gut Microbiota, and Stress-Related Metabolism in Free-Living Subjects"
Sunil Kochhar and colleagues note growing scientific evidence that antioxidants and other beneficial substances in dark chocolate may reduce risk factors for heart disease and other physical conditions. Studies also suggest that chocolate may ease emotional stress. Until now, however, there was little evidence from research in humans on exactly how chocolate might have those stress-busting effects.
In the study, scientists identified reductions in stress hormones and other stress-related biochemical changes in volunteers who rated themselves as highly stressed and ate dark chocolate for two weeks. "The study provides strong evidence that a daily consumption of 40 grams [1.4 ounces] during a period of 2 weeks is sufficient to modify the metabolism of healthy human volunteers," the scientists say.
"Metabolic Effects of Dark Chocolate Consumption on Energy, Gut Microbiota, and Stress-Related Metabolism in Free-Living Subjects"
Monday, November 9, 2009
Don't Get Vitamin D From The Sun
When it comes to vitamin D, consumers are bombarded with mixed messages about the best source for this essential nutrient. While some may argue that small doses of intentional sun exposure are safe, dermatologists point out that the risk of developing skin cancer from ultraviolet (UV) radiation far outweighs the benefit of stimulating vitamin D production – particularly when enriched foods and supplements are safe and effective sources of this vitamin.
“Despite years of ongoing public education efforts on the dangers of UV radiation, a number of misconceptions remain as to how to best protect ourselves from this known carcinogen and whether or not we absolutely need sun exposure for vitamin D production,” said Dr. Tanzi. “The fact is these myths are harmful because sun exposure is the leading cause of skin cancer, and the consequences of this misinformation could be potentially fatal.”
Myth: Sun exposure is the best source of vitamin D.
Vitamin D is an essential nutrient that is vital for strong bones and a healthy immune system. Deficiency of vitamin D is associated with bone softening in adults, rickets in children and, more recently, with high blood pressure, arthritis, type I diabetes and certain cancers.
While UV radiation is one source of vitamin D, dermatologists argue that it is not the best source because the benefits of obtaining vitamin D through UV exposure cannot be separated from an increased risk of skin cancer. Instead, the Academy recommends that an adequate amount of vitamin D should be obtained from a healthy diet that includes foods naturally rich in vitamin D (e.g., dairy products and fish), foods/beverages fortified with vitamin D (e.g., fortified milk and fortified cereals), and/or vitamin D supplements.
“Although studies showing the benefits of increased vitamin D intake have caused some to propose ‘sensible sun exposure’ or intentional sun exposure as a cost-effective method for preventing vitamin D deficiency, increased sun exposure is not the answer,” said Dr. Tanzi. “UV radiation is the most preventable risk factor for the development of skin cancer, which is the most common form of cancer in this country. There are more than an estimated 1 million new cases of skin cancer every year. Despite this fact, there remains a tremendous amount of misinformation about UV exposure – especially in relation to vitamin D.”
Myth: All sunscreens are created equal.
While on the surface most sunscreens may look the same, they are in fact quite different. One of the things that makes sunscreens different is the level of protection from UV exposure that they provide. Dr. Tanzi explained that a common misconception is that the SPF rates the degree of protection from both UVA rays (which pass through window glass, penetrate into the deepest layer of the skin and are associated with premature aging and melanoma) and UVB rays (the sun’s burning rays, which are blocked by window glass, are the primary cause of sunburn, and also are linked with skin cancer). In fact, the SPF number on sunscreens only reflects the product’s ability to deflect the sun’s burning rays (or UVB). Sunscreens labeled broad-spectrum provide coverage against both UVA and UVB light.
“SPF may create a false sense of security about the level of protection a person is getting, because many sunscreens do not adequately protect against harmful UVA rays,” said Dr. Tanzi. “The main challenge in providing effective protection from UVA rays is that traditional chemicals used in sunscreens that absorb UVA light degrade quickly and become ineffective.”
Fortunately, there are ingredients that can be added to traditional sunscreen ingredients to keep them stable and provide broad-spectrum protection. For example, Dr. Tanzi noted that the ingredient oxybenzone can help stabilize avobenzone (one of the best absorbers of UVA rays that, while highly effective, breaks down quickly), which provides a longer duration of effective protection from UVA rays. Other effective ingredients that help provide broad-spectrum UV coverage include ecamsule, cinoxate, menthyl anthranilate, octyl methoxycinnamate, octyl salicylate, and sulisobenzone.
For those with sensitive skin, sunscreens with non-chemical ingredients work best and will prevent irritation. Dr. Tanzi said the ingredients zinc oxide and titanium dioxide provide both UVA and UVB protection.
Myth: Using a higher SPF will ensure you don’t burn.
Dr. Tanzi explained that those who use sunscreen with a higher SPF may think they will not burn when exposed to UV light, but she said that is not true. In fact, actual sunscreen protection depends on many other factors – including skin type, the amount and frequency of sunscreen application, and the impact of activities (such as swimming and sweating). As a result, sunburn can occur even when wearing a higher SPF sunscreen.
Another important factor Dr. Tanzi emphasized is that UVB protection does not increase proportionately with a designated SPF number. For example, an SPF of 30 screens 97 percent of UVB rays, while an SPF of 15 screens 93 percent of UVB rays and an SPF of 2 screens out 50 percent of UVB rays. However, not applying enough sunscreen or not covering all exposed areas may result in a lower SPF than the product contains.
“For adequate protection, sunscreens are best applied 15-30 minutes prior to going outside, approximately every two hours or immediately after swimming or sweating,” said Dr. Tanzi. “Research demonstrates that most people only apply 25 to 50 percent of the recommended amount of sunscreen, which is one ounce for the entire body or enough to fill a shot glass. Therefore, if only half the proper amount of SPF 15 is applied, the SPF has been reduced to an SPF of approximately 5, which is then inadequate protection. ”
To address the issue of people not using enough sunscreen or reapplying improperly, the Academy recently increased its recommended SPF to a minimum of 30 for proper sun protection. Dr. Tanzi said that while sunscreen is important to protect against skin cancer, it is only one part of what should be an overall sun-protection program. To minimize your risk of skin cancer, the Academy recommends:
•Generously apply a broad-spectrum water-resistant sunscreen with a Sun Protection Factor (SPF) of at least 30 to all exposed skin. “Broad-spectrum” provides protection from both ultraviolet A (UVA) and ultraviolet B (UVB) rays. Re-apply approximately every two hours, even on cloudy days, and after swimming or sweating.
•Wear protective clothing, such as a long-sleeved shirt, pants, a wide-brimmed hat and sunglasses, where possible.
•Seek shade when appropriate, remembering that the sun's rays are strongest between 10 a.m. and 4 p.m. If your shadow is shorter than you are, seek shade.
•Protect children from sun exposure by playing in the shade, using protective clothing, and applying sunscreen.
•Use extra caution near water, snow and sand as they reflect the damaging rays of the sun which can increase your chance of sunburn.
•Get vitamin D safely through a healthy diet that may include vitamin supplements. Don't seek the sun.
•Avoid tanning beds. Ultraviolet light from the sun and tanning beds can cause skin cancer and wrinkling. If you want to look like you've been in the sun, consider using a sunless self-tanning product, but continue to use sunscreen with it.
•Check your birthday suit on your birthday. If you notice anything changing, growing, or bleeding on your skin, see a dermatologist. Skin cancer is very treatable when caught early.
“Despite years of ongoing public education efforts on the dangers of UV radiation, a number of misconceptions remain as to how to best protect ourselves from this known carcinogen and whether or not we absolutely need sun exposure for vitamin D production,” said Dr. Tanzi. “The fact is these myths are harmful because sun exposure is the leading cause of skin cancer, and the consequences of this misinformation could be potentially fatal.”
Myth: Sun exposure is the best source of vitamin D.
Vitamin D is an essential nutrient that is vital for strong bones and a healthy immune system. Deficiency of vitamin D is associated with bone softening in adults, rickets in children and, more recently, with high blood pressure, arthritis, type I diabetes and certain cancers.
While UV radiation is one source of vitamin D, dermatologists argue that it is not the best source because the benefits of obtaining vitamin D through UV exposure cannot be separated from an increased risk of skin cancer. Instead, the Academy recommends that an adequate amount of vitamin D should be obtained from a healthy diet that includes foods naturally rich in vitamin D (e.g., dairy products and fish), foods/beverages fortified with vitamin D (e.g., fortified milk and fortified cereals), and/or vitamin D supplements.
“Although studies showing the benefits of increased vitamin D intake have caused some to propose ‘sensible sun exposure’ or intentional sun exposure as a cost-effective method for preventing vitamin D deficiency, increased sun exposure is not the answer,” said Dr. Tanzi. “UV radiation is the most preventable risk factor for the development of skin cancer, which is the most common form of cancer in this country. There are more than an estimated 1 million new cases of skin cancer every year. Despite this fact, there remains a tremendous amount of misinformation about UV exposure – especially in relation to vitamin D.”
Myth: All sunscreens are created equal.
While on the surface most sunscreens may look the same, they are in fact quite different. One of the things that makes sunscreens different is the level of protection from UV exposure that they provide. Dr. Tanzi explained that a common misconception is that the SPF rates the degree of protection from both UVA rays (which pass through window glass, penetrate into the deepest layer of the skin and are associated with premature aging and melanoma) and UVB rays (the sun’s burning rays, which are blocked by window glass, are the primary cause of sunburn, and also are linked with skin cancer). In fact, the SPF number on sunscreens only reflects the product’s ability to deflect the sun’s burning rays (or UVB). Sunscreens labeled broad-spectrum provide coverage against both UVA and UVB light.
“SPF may create a false sense of security about the level of protection a person is getting, because many sunscreens do not adequately protect against harmful UVA rays,” said Dr. Tanzi. “The main challenge in providing effective protection from UVA rays is that traditional chemicals used in sunscreens that absorb UVA light degrade quickly and become ineffective.”
Fortunately, there are ingredients that can be added to traditional sunscreen ingredients to keep them stable and provide broad-spectrum protection. For example, Dr. Tanzi noted that the ingredient oxybenzone can help stabilize avobenzone (one of the best absorbers of UVA rays that, while highly effective, breaks down quickly), which provides a longer duration of effective protection from UVA rays. Other effective ingredients that help provide broad-spectrum UV coverage include ecamsule, cinoxate, menthyl anthranilate, octyl methoxycinnamate, octyl salicylate, and sulisobenzone.
For those with sensitive skin, sunscreens with non-chemical ingredients work best and will prevent irritation. Dr. Tanzi said the ingredients zinc oxide and titanium dioxide provide both UVA and UVB protection.
Myth: Using a higher SPF will ensure you don’t burn.
Dr. Tanzi explained that those who use sunscreen with a higher SPF may think they will not burn when exposed to UV light, but she said that is not true. In fact, actual sunscreen protection depends on many other factors – including skin type, the amount and frequency of sunscreen application, and the impact of activities (such as swimming and sweating). As a result, sunburn can occur even when wearing a higher SPF sunscreen.
Another important factor Dr. Tanzi emphasized is that UVB protection does not increase proportionately with a designated SPF number. For example, an SPF of 30 screens 97 percent of UVB rays, while an SPF of 15 screens 93 percent of UVB rays and an SPF of 2 screens out 50 percent of UVB rays. However, not applying enough sunscreen or not covering all exposed areas may result in a lower SPF than the product contains.
“For adequate protection, sunscreens are best applied 15-30 minutes prior to going outside, approximately every two hours or immediately after swimming or sweating,” said Dr. Tanzi. “Research demonstrates that most people only apply 25 to 50 percent of the recommended amount of sunscreen, which is one ounce for the entire body or enough to fill a shot glass. Therefore, if only half the proper amount of SPF 15 is applied, the SPF has been reduced to an SPF of approximately 5, which is then inadequate protection. ”
To address the issue of people not using enough sunscreen or reapplying improperly, the Academy recently increased its recommended SPF to a minimum of 30 for proper sun protection. Dr. Tanzi said that while sunscreen is important to protect against skin cancer, it is only one part of what should be an overall sun-protection program. To minimize your risk of skin cancer, the Academy recommends:
•Generously apply a broad-spectrum water-resistant sunscreen with a Sun Protection Factor (SPF) of at least 30 to all exposed skin. “Broad-spectrum” provides protection from both ultraviolet A (UVA) and ultraviolet B (UVB) rays. Re-apply approximately every two hours, even on cloudy days, and after swimming or sweating.
•Wear protective clothing, such as a long-sleeved shirt, pants, a wide-brimmed hat and sunglasses, where possible.
•Seek shade when appropriate, remembering that the sun's rays are strongest between 10 a.m. and 4 p.m. If your shadow is shorter than you are, seek shade.
•Protect children from sun exposure by playing in the shade, using protective clothing, and applying sunscreen.
•Use extra caution near water, snow and sand as they reflect the damaging rays of the sun which can increase your chance of sunburn.
•Get vitamin D safely through a healthy diet that may include vitamin supplements. Don't seek the sun.
•Avoid tanning beds. Ultraviolet light from the sun and tanning beds can cause skin cancer and wrinkling. If you want to look like you've been in the sun, consider using a sunless self-tanning product, but continue to use sunscreen with it.
•Check your birthday suit on your birthday. If you notice anything changing, growing, or bleeding on your skin, see a dermatologist. Skin cancer is very treatable when caught early.
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